TY  - JOUR
AU  - Radovanović, Marina
AU  - Lazarević, Nevena
AU  - Novaković, Jovana
AU  - Jeremić, Nevena
AU  - Jakovljević, Vladimir
AU  - Živković, Vladimir
AU  - Bradić, Jovana
AU  - Pecarski, Danijela
AU  - Tel-Çayan, Gülsen
AU  - Glamočlija, Jasmina
AU  - Soković, Marina
AU  - Gregori, Andrej
AU  - Petrović, Jovana
PY  - 2023
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5792
AB  - The present study aimed to examine the biological activity and cardioprotective potential of Trametes versicolor heteropolysaccharides (TVH) in a rat model of metabolic syndrome (MetS). This study included 40 Wistar rats divided into 5 groups: CTRL—healthy non-treated rats; MetS—non-treated rats; and H-TV, M-TV and L-TV-rats with MetS treated with either 300, 200 or 100 mg/kg TVH per os for 4 weeks. After finishing the treatment, we conducted an oral glucose tolerance test (OGTT), hemodynamic measurements and the animals were sacrificed, hearts isolated and subjected to the Langendorff technique. Blood samples were used for the determination of oxidative stress parameters, lipid status and insulin levels. We showed that α-amylase inhibition was not the mode of TVH antidiabetic action, while TVH showed a moderate inhibition of pathogenic microorganisms’ growth (MIC 8.00 mg·mL−1; MBC/MFC 16.00 mg·mL−1). H-TV and M-TV significantly reduced the level of prooxidants (O2−, H2O2, TBARS; p < 0.05), increased antioxidants activity (SOD, CAT, GSH; p < 0.05), reduced blood pressure (p < 0.05), improved glucose homeostasis in the OGTT test (p < 0.05), and ejection fraction (p < 0.05) and cardiac contractility (p < 0.05) compared to MetS (p < 0.05). Moreover, TVH treatment normalized the lipid status and decreased insulin levels compared to MetS rats (p < 0.05). The obtained results demonstrated that the TVH may be considered a useful agent for cardioprotection in MetS conditions.
PB  - Basel: MDPI
T2  - Pharmaceuticals
T1  - Characterization, In Vitro Biological Activity and In Vivo Cardioprotective Properties of Trametes versicolor (L.:Fr.) Quél. Heteropolysaccharides in a Rat Model of Metabolic Syndrome
IS  - 6
VL  - 16
DO  - 10.3390/ph16060787
SP  - 787
ER  - 

@article{
author = "Radovanović, Marina and Lazarević, Nevena and Novaković, Jovana and Jeremić, Nevena and Jakovljević, Vladimir and Živković, Vladimir and Bradić, Jovana and Pecarski, Danijela and Tel-Çayan, Gülsen and Glamočlija, Jasmina and Soković, Marina and Gregori, Andrej and Petrović, Jovana",
year = "2023",
abstract = "The present study aimed to examine the biological activity and cardioprotective potential of Trametes versicolor heteropolysaccharides (TVH) in a rat model of metabolic syndrome (MetS). This study included 40 Wistar rats divided into 5 groups: CTRL—healthy non-treated rats; MetS—non-treated rats; and H-TV, M-TV and L-TV-rats with MetS treated with either 300, 200 or 100 mg/kg TVH per os for 4 weeks. After finishing the treatment, we conducted an oral glucose tolerance test (OGTT), hemodynamic measurements and the animals were sacrificed, hearts isolated and subjected to the Langendorff technique. Blood samples were used for the determination of oxidative stress parameters, lipid status and insulin levels. We showed that α-amylase inhibition was not the mode of TVH antidiabetic action, while TVH showed a moderate inhibition of pathogenic microorganisms’ growth (MIC 8.00 mg·mL−1; MBC/MFC 16.00 mg·mL−1). H-TV and M-TV significantly reduced the level of prooxidants (O2−, H2O2, TBARS; p < 0.05), increased antioxidants activity (SOD, CAT, GSH; p < 0.05), reduced blood pressure (p < 0.05), improved glucose homeostasis in the OGTT test (p < 0.05), and ejection fraction (p < 0.05) and cardiac contractility (p < 0.05) compared to MetS (p < 0.05). Moreover, TVH treatment normalized the lipid status and decreased insulin levels compared to MetS rats (p < 0.05). The obtained results demonstrated that the TVH may be considered a useful agent for cardioprotection in MetS conditions.",
publisher = "Basel: MDPI",
journal = "Pharmaceuticals",
title = "Characterization, In Vitro Biological Activity and In Vivo Cardioprotective Properties of Trametes versicolor (L.:Fr.) Quél. Heteropolysaccharides in a Rat Model of Metabolic Syndrome",
number = "6",
volume = "16",
doi = "10.3390/ph16060787",
pages = "787"
}

Radovanović, M., Lazarević, N., Novaković, J., Jeremić, N., Jakovljević, V., Živković, V., Bradić, J., Pecarski, D., Tel-Çayan, G., Glamočlija, J., Soković, M., Gregori, A.,& Petrović, J.. (2023). Characterization, In Vitro Biological Activity and In Vivo Cardioprotective Properties of Trametes versicolor (L.:Fr.) Quél. Heteropolysaccharides in a Rat Model of Metabolic Syndrome. in Pharmaceuticals
Basel: MDPI., 16(6), 787.
https://doi.org/10.3390/ph16060787

Radovanović M, Lazarević N, Novaković J, Jeremić N, Jakovljević V, Živković V, Bradić J, Pecarski D, Tel-Çayan G, Glamočlija J, Soković M, Gregori A, Petrović J. Characterization, In Vitro Biological Activity and In Vivo Cardioprotective Properties of Trametes versicolor (L.:Fr.) Quél. Heteropolysaccharides in a Rat Model of Metabolic Syndrome. in Pharmaceuticals. 2023;16(6):787.
doi:10.3390/ph16060787 .

Radovanović, Marina, Lazarević, Nevena, Novaković, Jovana, Jeremić, Nevena, Jakovljević, Vladimir, Živković, Vladimir, Bradić, Jovana, Pecarski, Danijela, Tel-Çayan, Gülsen, Glamočlija, Jasmina, Soković, Marina, Gregori, Andrej, Petrović, Jovana, "Characterization, In Vitro Biological Activity and In Vivo Cardioprotective Properties of Trametes versicolor (L.:Fr.) Quél. Heteropolysaccharides in a Rat Model of Metabolic Syndrome" in Pharmaceuticals, 16, no. 6 (2023):787,
https://doi.org/10.3390/ph16060787 . .

TY  - CONF
AU  - Mićić, Bojana
AU  - Veličković, Nataša
AU  - Đorđević, Ana
AU  - Teofilović, Ana
AU  - Kovačević, Sanja
AU  - Radovanović, Marina
AU  - Brkljačić, Jelena
AU  - Macut Djuro
AU  - Vojnović Milutinović, Danijela
PY  - 2023
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6418
AB  - Introduction: Polycystic ovary syndrome (PCOS) is a common endocrine disorder that affects women’s
fertility and metabolic health throughout their life time. Insulin resistance and obesity, in conjunction
with excess androgens, are undeniably involved in its development. We aimed to elucidate how hyperandrogenemia
and prepubertal adiposity contribute to the development of metabolic disturbances in
rat model of PCOS.
Methods: The animal model of PCOS induced by 5a-dihydrotestosterone (DHT) was additionally challenged
by litter size reduction (LSR) during suckling period, to ensure overfeeding and development of
prepubertal adiposity. Systemic parameters of insulin sensitivity, along with markers of energy sensing,
insulin signaling, and lipid metabolism were analyzed in visceral adipose tissue (VAT) and skeletal muscle.
Results: The combination of treatments led to hyperinsulinemia and impaired systemic insulin sensitivity.
This was not accompanied with altered insulin signaling in the VAT, in spite of observed adipocytes
hypertrophy probably due to activation of AMPK and restrained lipogenesis in this tissue. On the other
hand, insulin signaling in skeletal muscle was impaired, which resulted in increased muscle fatty acid
uptake and oxidation after combined treatment. The switch to fatty acids oxidation subsequently led to
oxidative stress and inflammation, which was followed by adaptive activation of AMPK and increased
expression of its targets involved in antioxidant protection and mitochondrial biogenesis.
Conclusion: Our results suggest that prepubertal weight gain predisposes to insulin resistance development
in androgen-excess PCOS. The protective activation of AMPK in VAT and muscle makes it a potential
therapeutic target for insulin-resistant PCOS patients.
PB  - Belgrade: Institute of Molecular Genetics and Genetic Engineering, University of Belgrade
C3  - Abstract Book: CoMBoS2 - the Second Congress of Molecular Biologists of Serbia; 2023 Oct 6-8; Belgrade, Serbia
T1  - Metabolic disturbances in animal model of polycystic ovary syndrome: impact of early postnatal overfeeding
SP  - 144
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6418
ER  - 

@conference{
author = "Mićić, Bojana and Veličković, Nataša and Đorđević, Ana and Teofilović, Ana and Kovačević, Sanja and Radovanović, Marina and Brkljačić, Jelena and Macut Djuro and Vojnović Milutinović, Danijela",
year = "2023",
abstract = "Introduction: Polycystic ovary syndrome (PCOS) is a common endocrine disorder that affects women’s
fertility and metabolic health throughout their life time. Insulin resistance and obesity, in conjunction
with excess androgens, are undeniably involved in its development. We aimed to elucidate how hyperandrogenemia
and prepubertal adiposity contribute to the development of metabolic disturbances in
rat model of PCOS.
Methods: The animal model of PCOS induced by 5a-dihydrotestosterone (DHT) was additionally challenged
by litter size reduction (LSR) during suckling period, to ensure overfeeding and development of
prepubertal adiposity. Systemic parameters of insulin sensitivity, along with markers of energy sensing,
insulin signaling, and lipid metabolism were analyzed in visceral adipose tissue (VAT) and skeletal muscle.
Results: The combination of treatments led to hyperinsulinemia and impaired systemic insulin sensitivity.
This was not accompanied with altered insulin signaling in the VAT, in spite of observed adipocytes
hypertrophy probably due to activation of AMPK and restrained lipogenesis in this tissue. On the other
hand, insulin signaling in skeletal muscle was impaired, which resulted in increased muscle fatty acid
uptake and oxidation after combined treatment. The switch to fatty acids oxidation subsequently led to
oxidative stress and inflammation, which was followed by adaptive activation of AMPK and increased
expression of its targets involved in antioxidant protection and mitochondrial biogenesis.
Conclusion: Our results suggest that prepubertal weight gain predisposes to insulin resistance development
in androgen-excess PCOS. The protective activation of AMPK in VAT and muscle makes it a potential
therapeutic target for insulin-resistant PCOS patients.",
publisher = "Belgrade: Institute of Molecular Genetics and Genetic Engineering, University of Belgrade",
journal = "Abstract Book: CoMBoS2 - the Second Congress of Molecular Biologists of Serbia; 2023 Oct 6-8; Belgrade, Serbia",
title = "Metabolic disturbances in animal model of polycystic ovary syndrome: impact of early postnatal overfeeding",
pages = "144",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6418"
}

Mićić, B., Veličković, N., Đorđević, A., Teofilović, A., Kovačević, S., Radovanović, M., Brkljačić, J., Macut Djuro,& Vojnović Milutinović, D.. (2023). Metabolic disturbances in animal model of polycystic ovary syndrome: impact of early postnatal overfeeding. in Abstract Book: CoMBoS2 - the Second Congress of Molecular Biologists of Serbia; 2023 Oct 6-8; Belgrade, Serbia
Belgrade: Institute of Molecular Genetics and Genetic Engineering, University of Belgrade., 144.
https://hdl.handle.net/21.15107/rcub_ibiss_6418

Mićić B, Veličković N, Đorđević A, Teofilović A, Kovačević S, Radovanović M, Brkljačić J, Macut Djuro, Vojnović Milutinović D. Metabolic disturbances in animal model of polycystic ovary syndrome: impact of early postnatal overfeeding. in Abstract Book: CoMBoS2 - the Second Congress of Molecular Biologists of Serbia; 2023 Oct 6-8; Belgrade, Serbia. 2023;:144.
https://hdl.handle.net/21.15107/rcub_ibiss_6418 .

Mićić, Bojana, Veličković, Nataša, Đorđević, Ana, Teofilović, Ana, Kovačević, Sanja, Radovanović, Marina, Brkljačić, Jelena, Macut Djuro, Vojnović Milutinović, Danijela, "Metabolic disturbances in animal model of polycystic ovary syndrome: impact of early postnatal overfeeding" in Abstract Book: CoMBoS2 - the Second Congress of Molecular Biologists of Serbia; 2023 Oct 6-8; Belgrade, Serbia (2023):144,
https://hdl.handle.net/21.15107/rcub_ibiss_6418 .

TY  - JOUR
AU  - Radovanović, Marina
AU  - Kekić, Dusan
AU  - Gajić, Ina
AU  - Kabić, Jovana
AU  - Jovićević, Miloš
AU  - Kekić, Natalija
AU  - Opavski, Nataša
AU  - Ranin, Lazar
PY  - 2023
UR  - https://www.frontiersin.org/articles/10.3389/fnut.2023.1054555/full
UR  - http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC9928729
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5486
AB  - Antimicrobial resistance (AMR) poses a substantial threat to human health. The commensal bacteria of the gut microbiome were shown to serve as a reservoir of antibiotic resistance genes (ARGs), termed the gut resistome, which has the potential to transfer horizontally to pathogens and contribute to the emergence of drug-resistant bacteria. Namely, AMR traits are generally linked with mobile genetic elements (MGEs), which apart from disseminating vertically to the progeny, may cross horizontally to the distantly related microbial species. On the other hand, while probiotics are generally considered beneficiary to human health, and are therefore widely consumed in recent years most commonly in conjunction with antibiotics, the complexities and extent of their impact on the gut microbiome and resistome have not been elucidated. By reviewing the latest studies on ARG containing commercial probiotic products and common probiotic supplement species with their actual effects on the human gut resistome, this study aims to demonstrate that their contribution to the spread of ARGs along the GI tract merits additional attention, but also indicates the changes in sampling and profiling of the gut microbiome which may allow for the more comprehensive studying of the effects of probiotics in this part of the resistome.
PB  - Frontiers Media S.A.
T2  - Frontiers in Nutrition
T1  - Potential influence of antimicrobial resistance gene content in probiotic bacteria on the gut resistome ecosystems
VL  - 10
DO  - 10.3389/fnut.2023.1054555
SP  - 1054555
ER  - 

@article{
author = "Radovanović, Marina and Kekić, Dusan and Gajić, Ina and Kabić, Jovana and Jovićević, Miloš and Kekić, Natalija and Opavski, Nataša and Ranin, Lazar",
year = "2023",
abstract = "Antimicrobial resistance (AMR) poses a substantial threat to human health. The commensal bacteria of the gut microbiome were shown to serve as a reservoir of antibiotic resistance genes (ARGs), termed the gut resistome, which has the potential to transfer horizontally to pathogens and contribute to the emergence of drug-resistant bacteria. Namely, AMR traits are generally linked with mobile genetic elements (MGEs), which apart from disseminating vertically to the progeny, may cross horizontally to the distantly related microbial species. On the other hand, while probiotics are generally considered beneficiary to human health, and are therefore widely consumed in recent years most commonly in conjunction with antibiotics, the complexities and extent of their impact on the gut microbiome and resistome have not been elucidated. By reviewing the latest studies on ARG containing commercial probiotic products and common probiotic supplement species with their actual effects on the human gut resistome, this study aims to demonstrate that their contribution to the spread of ARGs along the GI tract merits additional attention, but also indicates the changes in sampling and profiling of the gut microbiome which may allow for the more comprehensive studying of the effects of probiotics in this part of the resistome.",
publisher = "Frontiers Media S.A.",
journal = "Frontiers in Nutrition",
title = "Potential influence of antimicrobial resistance gene content in probiotic bacteria on the gut resistome ecosystems",
volume = "10",
doi = "10.3389/fnut.2023.1054555",
pages = "1054555"
}

Radovanović, M., Kekić, D., Gajić, I., Kabić, J., Jovićević, M., Kekić, N., Opavski, N.,& Ranin, L.. (2023). Potential influence of antimicrobial resistance gene content in probiotic bacteria on the gut resistome ecosystems. in Frontiers in Nutrition
Frontiers Media S.A.., 10, 1054555.
https://doi.org/10.3389/fnut.2023.1054555

Radovanović M, Kekić D, Gajić I, Kabić J, Jovićević M, Kekić N, Opavski N, Ranin L. Potential influence of antimicrobial resistance gene content in probiotic bacteria on the gut resistome ecosystems. in Frontiers in Nutrition. 2023;10:1054555.
doi:10.3389/fnut.2023.1054555 .

Radovanović, Marina, Kekić, Dusan, Gajić, Ina, Kabić, Jovana, Jovićević, Miloš, Kekić, Natalija, Opavski, Nataša, Ranin, Lazar, "Potential influence of antimicrobial resistance gene content in probiotic bacteria on the gut resistome ecosystems" in Frontiers in Nutrition, 10 (2023):1054555,
https://doi.org/10.3389/fnut.2023.1054555 . .

TY  - JOUR
AU  - Radovanović, Marina
AU  - Kekić, Dušan
AU  - Jovičević, Miloš
AU  - Kabić, Jovana
AU  - Gajić, Ina
AU  - Opavski, Nataša
AU  - Ranin, Lazar
PY  - 2022
UR  - http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC9697523
UR  - https://www.mdpi.com/2076-0817/11/11/1230
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5240
AB  - Neisseria gonorrhoeae (N. gonorrhoeae) is the etiological agent of the second most common sexually transmitted disease in the world, gonorrhoea. Currently recommended and last available first-line therapy is extended-spectrum cephalosporins most often combined with azitromycin. However, misuse of antibiotics and the abilities of N. gonorrhoeae to acquire new genetic and plasmid-borne resistance determinants has gradually led to the situation where this bacterium has become resistant to all major classes of antibiotics. Together with a generally slow update of treatment guidelines globally, as well as with the high capacity of gonococci to develop and retain AMR, this may lead to the global worsening of gonococcal AMR. Since effective vaccines are unavailable, the management of gonorrhoea relies mostly on prevention and accurate diagnosis, together with antimicrobial treatment. The study overviews the latest results of mostly WHO-initiated studies, primarily focusing on the data regarding the molecular basis of the resistance to the current and novel most promising antibacterial agents, which could serve to establish or reinforce the continual, quality-assured and comparable AMR surveillance, including systematic monitoring and treatment with the use of molecular AMR prediction methods.
PB  - Basel: MDPI
T2  - Pathogens
T1  - Current Susceptibility Surveillance and Distribution of Antimicrobial Resistance in N. gonorrheae within WHO Regions
IS  - 11
VL  - 11
DO  - 10.3390/pathogens11111230
SP  - 1230
ER  - 

@article{
author = "Radovanović, Marina and Kekić, Dušan and Jovičević, Miloš and Kabić, Jovana and Gajić, Ina and Opavski, Nataša and Ranin, Lazar",
year = "2022",
abstract = "Neisseria gonorrhoeae (N. gonorrhoeae) is the etiological agent of the second most common sexually transmitted disease in the world, gonorrhoea. Currently recommended and last available first-line therapy is extended-spectrum cephalosporins most often combined with azitromycin. However, misuse of antibiotics and the abilities of N. gonorrhoeae to acquire new genetic and plasmid-borne resistance determinants has gradually led to the situation where this bacterium has become resistant to all major classes of antibiotics. Together with a generally slow update of treatment guidelines globally, as well as with the high capacity of gonococci to develop and retain AMR, this may lead to the global worsening of gonococcal AMR. Since effective vaccines are unavailable, the management of gonorrhoea relies mostly on prevention and accurate diagnosis, together with antimicrobial treatment. The study overviews the latest results of mostly WHO-initiated studies, primarily focusing on the data regarding the molecular basis of the resistance to the current and novel most promising antibacterial agents, which could serve to establish or reinforce the continual, quality-assured and comparable AMR surveillance, including systematic monitoring and treatment with the use of molecular AMR prediction methods.",
publisher = "Basel: MDPI",
journal = "Pathogens",
title = "Current Susceptibility Surveillance and Distribution of Antimicrobial Resistance in N. gonorrheae within WHO Regions",
number = "11",
volume = "11",
doi = "10.3390/pathogens11111230",
pages = "1230"
}

Radovanović, M., Kekić, D., Jovičević, M., Kabić, J., Gajić, I., Opavski, N.,& Ranin, L.. (2022). Current Susceptibility Surveillance and Distribution of Antimicrobial Resistance in N. gonorrheae within WHO Regions. in Pathogens
Basel: MDPI., 11(11), 1230.
https://doi.org/10.3390/pathogens11111230

Radovanović M, Kekić D, Jovičević M, Kabić J, Gajić I, Opavski N, Ranin L. Current Susceptibility Surveillance and Distribution of Antimicrobial Resistance in N. gonorrheae within WHO Regions. in Pathogens. 2022;11(11):1230.
doi:10.3390/pathogens11111230 .

Radovanović, Marina, Kekić, Dušan, Jovičević, Miloš, Kabić, Jovana, Gajić, Ina, Opavski, Nataša, Ranin, Lazar, "Current Susceptibility Surveillance and Distribution of Antimicrobial Resistance in N. gonorrheae within WHO Regions" in Pathogens, 11, no. 11 (2022):1230,
https://doi.org/10.3390/pathogens11111230 . .

TY  - CONF
AU  - Mićić, Bojana
AU  - Radovanović, Marina
AU  - Tovilović-Kovačević, Gordana
AU  - Teofilović, Ana
AU  - Gligorovska, Ljupka
AU  - Vojnović-Milutinović, Danijela
AU  - Đorđević, Ana
AU  - Ignjatović, Đurđica
PY  - 2021
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/4718
AB  - Fructose intake is associated with low-grade inflammation and increased oxidative
stress. Among long chain polyunsaturated fatty acids (LC-PUFAs), Ω-6 are recognized as a
contributing factor to inflammation, while Ω-3 LC-PUFAs are considered as functional foods with
beneficial effects, including inhibition of pro-inflammatory pathways. The aim of this study was to
analyze combined effects of physiologically relevant LC-PUFAs and fructose on inflammation and
antioxidant enzymes in the in vitro model of vascular endothelial cells. We examined the effects
of 0.5 mM fructose, alone and in combination with Ω-6 (arachidonic (AA) and linoleic (LA)) and
Ω-3 (eicosapentaenoic (EPA) and docosahexaenoic acid (DHA)) LC-PUFAs on expression of pro-
inflammatory cytokines (tumor necrosis factor α (TNFα) and interleukin 6 (IL6)) in EA.hy926 cells.
The protein levels of nuclear factor-κB (NF-κB) and IB, as well as its phosphorylation, together
with superoxide dismutase (SOD) 1 and 2, catalase and glutathione reductase (GR) were also
analyzed. Total ROS amounts were determined using flow cytometric analysis of cells stained
with redox sensitive dihydrorhodamine 123 dye. The results showed that treatment of cells with
fructose increased TNFα and decreased IL6 mRNA levels. Additional treatment with LA, DHA
and EPA reduced TNFα and led to further decrease of IL6 expression. The observed changes
were not associated with NFB activation. All examined enzymes were unchanged after fructose
treatment, while GR was increased by LC-PUFA addition. SOD2 was reduced in cells treated
with AA, LA and EPA, while increased ROS amounts were observed with AA, DHA and EPA. This
was also evident in combined treatment with fructose. These preliminary results suggest that
LC-PUFAs, besides effect on pro-inflammatory cytokines, reduce SOD2 levels and increase ROS.
The increased levels of ROS could stimulate production of PUFA-derived peroxides, which in
GSH-enriched environment might be converted into anti-inflammatory derivatives, additionally
suppressing inflammation in fructose treated endothelial cells
PB  - Elsevier Inc.
C3  - Free Radical Research Europe (SFRR-E) Annual Meeting Abstracts “Redox biology in the 21st century: a new scientific discipline” 15-18 June 2021, Belgrade, Serbia
T1  - Potentiation of polyunsaturated fatty acids anti-inflammatory action through redox signaling in fructose-treated endothelial cells
DO  - 10.1016/j.freeradbiomed.2021.08.092
SP  - S79
ER  - 

@conference{
author = "Mićić, Bojana and Radovanović, Marina and Tovilović-Kovačević, Gordana and Teofilović, Ana and Gligorovska, Ljupka and Vojnović-Milutinović, Danijela and Đorđević, Ana and Ignjatović, Đurđica",
year = "2021",
abstract = "Fructose intake is associated with low-grade inflammation and increased oxidative
stress. Among long chain polyunsaturated fatty acids (LC-PUFAs), Ω-6 are recognized as a
contributing factor to inflammation, while Ω-3 LC-PUFAs are considered as functional foods with
beneficial effects, including inhibition of pro-inflammatory pathways. The aim of this study was to
analyze combined effects of physiologically relevant LC-PUFAs and fructose on inflammation and
antioxidant enzymes in the in vitro model of vascular endothelial cells. We examined the effects
of 0.5 mM fructose, alone and in combination with Ω-6 (arachidonic (AA) and linoleic (LA)) and
Ω-3 (eicosapentaenoic (EPA) and docosahexaenoic acid (DHA)) LC-PUFAs on expression of pro-
inflammatory cytokines (tumor necrosis factor α (TNFα) and interleukin 6 (IL6)) in EA.hy926 cells.
The protein levels of nuclear factor-κB (NF-κB) and IB, as well as its phosphorylation, together
with superoxide dismutase (SOD) 1 and 2, catalase and glutathione reductase (GR) were also
analyzed. Total ROS amounts were determined using flow cytometric analysis of cells stained
with redox sensitive dihydrorhodamine 123 dye. The results showed that treatment of cells with
fructose increased TNFα and decreased IL6 mRNA levels. Additional treatment with LA, DHA
and EPA reduced TNFα and led to further decrease of IL6 expression. The observed changes
were not associated with NFB activation. All examined enzymes were unchanged after fructose
treatment, while GR was increased by LC-PUFA addition. SOD2 was reduced in cells treated
with AA, LA and EPA, while increased ROS amounts were observed with AA, DHA and EPA. This
was also evident in combined treatment with fructose. These preliminary results suggest that
LC-PUFAs, besides effect on pro-inflammatory cytokines, reduce SOD2 levels and increase ROS.
The increased levels of ROS could stimulate production of PUFA-derived peroxides, which in
GSH-enriched environment might be converted into anti-inflammatory derivatives, additionally
suppressing inflammation in fructose treated endothelial cells",
publisher = "Elsevier Inc.",
journal = "Free Radical Research Europe (SFRR-E) Annual Meeting Abstracts “Redox biology in the 21st century: a new scientific discipline” 15-18 June 2021, Belgrade, Serbia",
title = "Potentiation of polyunsaturated fatty acids anti-inflammatory action through redox signaling in fructose-treated endothelial cells",
doi = "10.1016/j.freeradbiomed.2021.08.092",
pages = "S79"
}

Mićić, B., Radovanović, M., Tovilović-Kovačević, G., Teofilović, A., Gligorovska, L., Vojnović-Milutinović, D., Đorđević, A.,& Ignjatović, Đ.. (2021). Potentiation of polyunsaturated fatty acids anti-inflammatory action through redox signaling in fructose-treated endothelial cells. in Free Radical Research Europe (SFRR-E) Annual Meeting Abstracts “Redox biology in the 21st century: a new scientific discipline” 15-18 June 2021, Belgrade, Serbia
Elsevier Inc.., S79.
https://doi.org/10.1016/j.freeradbiomed.2021.08.092

Mićić B, Radovanović M, Tovilović-Kovačević G, Teofilović A, Gligorovska L, Vojnović-Milutinović D, Đorđević A, Ignjatović Đ. Potentiation of polyunsaturated fatty acids anti-inflammatory action through redox signaling in fructose-treated endothelial cells. in Free Radical Research Europe (SFRR-E) Annual Meeting Abstracts “Redox biology in the 21st century: a new scientific discipline” 15-18 June 2021, Belgrade, Serbia. 2021;:S79.
doi:10.1016/j.freeradbiomed.2021.08.092 .

Mićić, Bojana, Radovanović, Marina, Tovilović-Kovačević, Gordana, Teofilović, Ana, Gligorovska, Ljupka, Vojnović-Milutinović, Danijela, Đorđević, Ana, Ignjatović, Đurđica, "Potentiation of polyunsaturated fatty acids anti-inflammatory action through redox signaling in fructose-treated endothelial cells" in Free Radical Research Europe (SFRR-E) Annual Meeting Abstracts “Redox biology in the 21st century: a new scientific discipline” 15-18 June 2021, Belgrade, Serbia (2021):S79,
https://doi.org/10.1016/j.freeradbiomed.2021.08.092 . .

TY  - JOUR
AU  - Vojnović-Milutinović, Danijela
AU  - Brkljačić, Jelena
AU  - Teofilović, Ana
AU  - Bursać, Biljana
AU  - Radovanović, Marina
AU  - Gligorovska, Ljupka
AU  - Kovačević, Sanja
AU  - Đorđević, Ana
AU  - Preitner, Frederic
AU  - Tappy, Luc
AU  - Matić, Gordana
AU  - Veličković, Nataša
PY  - 2020
UR  - https://onlinelibrary.wiley.com/doi/abs/10.1002/mnfr.201901141
UR  - http://www.ncbi.nlm.nih.gov/pubmed/32379936
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3702
AB  - SCOPE Intake of fructose-sweetened beverages and chronic stress (CS) both increase risk of cardiometabolic diseases. The aim is to investigate whether these factors synergistically perturb lipid metabolism in rat liver and kidney. METHODS AND RESULTS Fractional de novo lipogenesis (fDNL), intrahepatic- and intrarenal-triglycerides (IHTG and IRTG), de novo palmitate (DNPalm) content, FA composition, VLDL-TGs kinetics, and key metabolic gene expression at the end of the feeding and non-feeding phases in rats exposed to standard chow diet, chow diet + CS, 20% liquid high-fructose supplementation (HFr), or HFr+CS are measured. HFr induces hypertriglyceridemia, up-regulates fructose-metabolism and gluconeogenic enzymes, increases IHTG and DNPalm content in IHTG and IRTG, and augments fDNL at the end of the feeding phase. These changes are diminished after the non-feeding phase. CS does not exert such effects, but when combined with HFr, it reduces IHTG and visceral adiposity, enhances lipogenic gene expression and fDNL, and increases VLDL-DNPalm secretion. CONCLUSION Liquid high-fructose supplementation increases IHTG and VLDL-TG secretion after the feeding phase, the latter being the result of stimulated hepatic and renal DNL. Chronic stress potentiates the effects of high fructose on fDNL and export of newly synthesized VLDL-TGs, and decreases fructose-induced intrahepatic TG accumulation after the feeding phase.
PB  - John Wiley & Sons, Ltd
T2  - Molecular Nutrition & Food Research
T1  - Chronic Stress Potentiates High Fructose-Induced Lipogenesis in Rat Liver and Kidney.
IS  - 13
VL  - 64
DO  - 10.1002/mnfr.201901141
SP  - e1901141
ER  - 

@article{
author = "Vojnović-Milutinović, Danijela and Brkljačić, Jelena and Teofilović, Ana and Bursać, Biljana and Radovanović, Marina and Gligorovska, Ljupka and Kovačević, Sanja and Đorđević, Ana and Preitner, Frederic and Tappy, Luc and Matić, Gordana and Veličković, Nataša",
year = "2020",
abstract = "SCOPE Intake of fructose-sweetened beverages and chronic stress (CS) both increase risk of cardiometabolic diseases. The aim is to investigate whether these factors synergistically perturb lipid metabolism in rat liver and kidney. METHODS AND RESULTS Fractional de novo lipogenesis (fDNL), intrahepatic- and intrarenal-triglycerides (IHTG and IRTG), de novo palmitate (DNPalm) content, FA composition, VLDL-TGs kinetics, and key metabolic gene expression at the end of the feeding and non-feeding phases in rats exposed to standard chow diet, chow diet + CS, 20% liquid high-fructose supplementation (HFr), or HFr+CS are measured. HFr induces hypertriglyceridemia, up-regulates fructose-metabolism and gluconeogenic enzymes, increases IHTG and DNPalm content in IHTG and IRTG, and augments fDNL at the end of the feeding phase. These changes are diminished after the non-feeding phase. CS does not exert such effects, but when combined with HFr, it reduces IHTG and visceral adiposity, enhances lipogenic gene expression and fDNL, and increases VLDL-DNPalm secretion. CONCLUSION Liquid high-fructose supplementation increases IHTG and VLDL-TG secretion after the feeding phase, the latter being the result of stimulated hepatic and renal DNL. Chronic stress potentiates the effects of high fructose on fDNL and export of newly synthesized VLDL-TGs, and decreases fructose-induced intrahepatic TG accumulation after the feeding phase.",
publisher = "John Wiley & Sons, Ltd",
journal = "Molecular Nutrition & Food Research",
title = "Chronic Stress Potentiates High Fructose-Induced Lipogenesis in Rat Liver and Kidney.",
number = "13",
volume = "64",
doi = "10.1002/mnfr.201901141",
pages = "e1901141"
}

Vojnović-Milutinović, D., Brkljačić, J., Teofilović, A., Bursać, B., Radovanović, M., Gligorovska, L., Kovačević, S., Đorđević, A., Preitner, F., Tappy, L., Matić, G.,& Veličković, N.. (2020). Chronic Stress Potentiates High Fructose-Induced Lipogenesis in Rat Liver and Kidney.. in Molecular Nutrition & Food Research
John Wiley & Sons, Ltd., 64(13), e1901141.
https://doi.org/10.1002/mnfr.201901141

Vojnović-Milutinović D, Brkljačić J, Teofilović A, Bursać B, Radovanović M, Gligorovska L, Kovačević S, Đorđević A, Preitner F, Tappy L, Matić G, Veličković N. Chronic Stress Potentiates High Fructose-Induced Lipogenesis in Rat Liver and Kidney.. in Molecular Nutrition & Food Research. 2020;64(13):e1901141.
doi:10.1002/mnfr.201901141 .

Vojnović-Milutinović, Danijela, Brkljačić, Jelena, Teofilović, Ana, Bursać, Biljana, Radovanović, Marina, Gligorovska, Ljupka, Kovačević, Sanja, Đorđević, Ana, Preitner, Frederic, Tappy, Luc, Matić, Gordana, Veličković, Nataša, "Chronic Stress Potentiates High Fructose-Induced Lipogenesis in Rat Liver and Kidney." in Molecular Nutrition & Food Research, 64, no. 13 (2020):e1901141,
https://doi.org/10.1002/mnfr.201901141 . .

TY  - CONF
AU  - Veličković, Nataša
AU  - Vojnović-Milutinović, Danijela
AU  - Brkljačić, Jelena
AU  - Teofilović, Ana
AU  - Bursać, Biljana
AU  - Radovanović, Marina
AU  - Gligorovska, Ljupka
AU  - Kovačević, Sanja
AU  - Đorđević, Ana
AU  - Preitner, Frédéric
AU  - Tappy, Luc
AU  - Matić, Gordana
PY  - 2020
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4117
AB  - Overconsumption of fructoseenriched beverages and everyday stress are
both involved in the pathogenesis of metabolic disorders through their effects
on hepatic lipid metabolism. The aim of this study was to investigate
whether highfructose diet and chronic stress synergistically perturbs lipid
metabolism in rat liver. Therefore, we analyzed the effects of 9-week
20% liquid fructose diet and 4-week chronic unpredictable stress, separately
and in combination, on dyslipidemia, VLDL-TG kinetics, intrahepatic
triglycerides (IHTG), liver de novo palmitate (DNPalm) content and fatty
acid (FA) composition. In parallel, hepatic fractional de novo lipogenesis
(fDNL) by stable isotope tracer protocol, as well as expression of lipid metabolism
regulators were also analyzed. Results showed that highfructose
diet led to hypertriglyceridemia, increased plasma VLDL-TGs and free FA
(FFA), and increased visceral adiposity. Fructose diet also augmented the level of palmitate, palmitoleate and oleate in the liver, the latter being result
of increased desaturase activity. In addition, newly synthesized palmitate
(DNPalm content) was increased in the liver of fructose-fed animals,
most likely as a result of stimulated fDNL. Chronic stress alone did not
exert such effects, but when combined with fructose, stress decreased FFA
level, ameliorated fructose-induced TG accumulation, and augmented the
release of VLDL-TGs. Stress also enhanced the effects of high-fructose
diet on fDNL, which was accompanied with increased expression of key
regulators of lipid metabolism, that resulting in stimulated export of newly
synthesized palmitate in the form of VLDL-TGs. These results imply that
high-fructose diet affects hepatic lipid metabolism by stimulating fDNL
and increasing de novo synthesized palmitate, which is partially accumulated
in the liver and in part released into circulation in the form of VLDLTGs.
On the other hand, stress in combination with high-fructose diet
potentiated hepatic fDNL, but it decreased temporary TG storage and redirected
newly synthesized palmitate into VLDL-TGs. Thus, the combination
of high-fructose diet and chronic stress, as hallmarks of modern lifestyle,
exerts more detrimental influence on lipid homeostasis than the individual
factors, judged by stimulated fDNL and increased export of VLDL-TGs to
non-hepatic tissues.
PB  - European Society of Endocrinology
C3  - 22nd European Congress of Endocrinology; 2020 Sep 5-9
T1  - Fructose-induced alterations of hepatic lipid metabolism are modulated by chronic stress in male rats
DO  - 10.1530/endoabs.70.AEP435
SP  - AEP435
ER  - 

@conference{
author = "Veličković, Nataša and Vojnović-Milutinović, Danijela and Brkljačić, Jelena and Teofilović, Ana and Bursać, Biljana and Radovanović, Marina and Gligorovska, Ljupka and Kovačević, Sanja and Đorđević, Ana and Preitner, Frédéric and Tappy, Luc and Matić, Gordana",
year = "2020",
abstract = "Overconsumption of fructoseenriched beverages and everyday stress are
both involved in the pathogenesis of metabolic disorders through their effects
on hepatic lipid metabolism. The aim of this study was to investigate
whether highfructose diet and chronic stress synergistically perturbs lipid
metabolism in rat liver. Therefore, we analyzed the effects of 9-week
20% liquid fructose diet and 4-week chronic unpredictable stress, separately
and in combination, on dyslipidemia, VLDL-TG kinetics, intrahepatic
triglycerides (IHTG), liver de novo palmitate (DNPalm) content and fatty
acid (FA) composition. In parallel, hepatic fractional de novo lipogenesis
(fDNL) by stable isotope tracer protocol, as well as expression of lipid metabolism
regulators were also analyzed. Results showed that highfructose
diet led to hypertriglyceridemia, increased plasma VLDL-TGs and free FA
(FFA), and increased visceral adiposity. Fructose diet also augmented the level of palmitate, palmitoleate and oleate in the liver, the latter being result
of increased desaturase activity. In addition, newly synthesized palmitate
(DNPalm content) was increased in the liver of fructose-fed animals,
most likely as a result of stimulated fDNL. Chronic stress alone did not
exert such effects, but when combined with fructose, stress decreased FFA
level, ameliorated fructose-induced TG accumulation, and augmented the
release of VLDL-TGs. Stress also enhanced the effects of high-fructose
diet on fDNL, which was accompanied with increased expression of key
regulators of lipid metabolism, that resulting in stimulated export of newly
synthesized palmitate in the form of VLDL-TGs. These results imply that
high-fructose diet affects hepatic lipid metabolism by stimulating fDNL
and increasing de novo synthesized palmitate, which is partially accumulated
in the liver and in part released into circulation in the form of VLDLTGs.
On the other hand, stress in combination with high-fructose diet
potentiated hepatic fDNL, but it decreased temporary TG storage and redirected
newly synthesized palmitate into VLDL-TGs. Thus, the combination
of high-fructose diet and chronic stress, as hallmarks of modern lifestyle,
exerts more detrimental influence on lipid homeostasis than the individual
factors, judged by stimulated fDNL and increased export of VLDL-TGs to
non-hepatic tissues.",
publisher = "European Society of Endocrinology",
journal = "22nd European Congress of Endocrinology; 2020 Sep 5-9",
title = "Fructose-induced alterations of hepatic lipid metabolism are modulated by chronic stress in male rats",
doi = "10.1530/endoabs.70.AEP435",
pages = "AEP435"
}

Veličković, N., Vojnović-Milutinović, D., Brkljačić, J., Teofilović, A., Bursać, B., Radovanović, M., Gligorovska, L., Kovačević, S., Đorđević, A., Preitner, F., Tappy, L.,& Matić, G.. (2020). Fructose-induced alterations of hepatic lipid metabolism are modulated by chronic stress in male rats. in 22nd European Congress of Endocrinology; 2020 Sep 5-9
European Society of Endocrinology., AEP435.
https://doi.org/10.1530/endoabs.70.AEP435

Veličković N, Vojnović-Milutinović D, Brkljačić J, Teofilović A, Bursać B, Radovanović M, Gligorovska L, Kovačević S, Đorđević A, Preitner F, Tappy L, Matić G. Fructose-induced alterations of hepatic lipid metabolism are modulated by chronic stress in male rats. in 22nd European Congress of Endocrinology; 2020 Sep 5-9. 2020;:AEP435.
doi:10.1530/endoabs.70.AEP435 .

Veličković, Nataša, Vojnović-Milutinović, Danijela, Brkljačić, Jelena, Teofilović, Ana, Bursać, Biljana, Radovanović, Marina, Gligorovska, Ljupka, Kovačević, Sanja, Đorđević, Ana, Preitner, Frédéric, Tappy, Luc, Matić, Gordana, "Fructose-induced alterations of hepatic lipid metabolism are modulated by chronic stress in male rats" in 22nd European Congress of Endocrinology; 2020 Sep 5-9 (2020):AEP435,
https://doi.org/10.1530/endoabs.70.AEP435 . .

TY  - CONF
AU  - Vojnović-Milutinović, Danijela
AU  - Veličković, Nataša
AU  - Radovanović, Marina
AU  - Đorđević, Ana
AU  - Brkljačić, Jelena
AU  - Teofilović, Ana
AU  - Bursać, Biljana
AU  - Jelača, Sanja
AU  - Macut, Đuro
PY  - 2020
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4116
AB  - Polycystic ovary syndrome (PCOS) is a complex reproductive disorder that
is usually associated with metabolic disturbances such as obesity, dyslipidemia
and insulin resistance. In this study, female rats treated with nonaromatizable
5α dihydrotestosterone (DHT) were used as an animal model of
PCOS. The aim of this study was to assess the presence of inflammation in liver and visceral adipose tissue (VAT), which accompanies metabolic
disturbances in animal model of PCOS. Female (21 days old) Wistar rats
were treated subcutaneously with DHT pellets, while control animals received
placebo pellets. Glucose, triglycerides, free fatty acids (FFA) were
determined in blood plasma, while corticosterone was analyzed both in plasma
and liver. Expression of genes and proteinsinvolved in lipid metabolism,
such as sterol regulatory element binding protein1 (SREBP-1), fatty acid
synthase (FAS) and acetyl-CoA carboxylase (ACC), lipin-1, adipose tissue
triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), were analyzed
in the VAT of treated rats. Tissue inflammationevaluated by nuclear
factor kappa B (NFκB)protein level and intracellular distribution, as well as
by TNFα, IL6 and IL1β mRNA levels. Glucocorticoid signaling was examined
at the level of 11 beta hydroxysteroid dehydrogenase type 1 (11βHSD1)
and 5α-reductase, as well asby glucocorticoid receptor (GR) leveland its
subcellular distribution. The results showed that DHT treatment induced increase
of lipogenic factors (SREBP-1, lipin-1, FAS and PEPCK), while the
level of lipolytic enzyme HSL was decreasedin VAT. These molecular alterations
were accompanied by adipocyte hypertrophy, visceral obesity and
elevated plasma FFA and triglyceride concentrations. Those changes in lipid
metabolism were possible trigger for low-grade inflammation observed in
the VAT and characterized by NFκB activation and increasedIL6 and IL1β
mRNA levels. In spite of increased VAT proinflammatory mediators, the
level of proinflammatory cytokines, IL6 and IL1β, was decreased in the liver
of DHT-treated rats, while the activation of NFκB remained unchanged.
The state of suppressed inflammation in the liver could be an outcome of
stimulated glucocorticoid signaling, as judged byincreased hepatic corticosterone
level and GR activation. The augmentation of hepatic glucocorticoids
could be a net result of increased expression of 11βHSD1 and decreased
expression of 5β-reductase mRNA. In conclusion, the results showed that
abdominal obesity and dyslipidemia in the animal model of PCOS were accompanied
with hypertrophic adipocytes, lipid accumulation and low-grade
inflammation in the VAT. However, these metabolic disturbances did not resultin
hepatic inflammation due to increased tissue levels of glucocorticoids.
PB  - European Society of Endocrinology
C3  - 22nd European Congress of Endocrinology: Abstracts; 2020 Sep 5-9
T1  - Different effects of 5α-dihydrotestosterone treatment on hepatic and visceral adipose tissue inflammation in animal model of polycystic ovary syndrome
DO  - 10.1530/endoabs.70.AEP382
SP  - AEP382
ER  - 

@conference{
author = "Vojnović-Milutinović, Danijela and Veličković, Nataša and Radovanović, Marina and Đorđević, Ana and Brkljačić, Jelena and Teofilović, Ana and Bursać, Biljana and Jelača, Sanja and Macut, Đuro",
year = "2020",
abstract = "Polycystic ovary syndrome (PCOS) is a complex reproductive disorder that
is usually associated with metabolic disturbances such as obesity, dyslipidemia
and insulin resistance. In this study, female rats treated with nonaromatizable
5α dihydrotestosterone (DHT) were used as an animal model of
PCOS. The aim of this study was to assess the presence of inflammation in liver and visceral adipose tissue (VAT), which accompanies metabolic
disturbances in animal model of PCOS. Female (21 days old) Wistar rats
were treated subcutaneously with DHT pellets, while control animals received
placebo pellets. Glucose, triglycerides, free fatty acids (FFA) were
determined in blood plasma, while corticosterone was analyzed both in plasma
and liver. Expression of genes and proteinsinvolved in lipid metabolism,
such as sterol regulatory element binding protein1 (SREBP-1), fatty acid
synthase (FAS) and acetyl-CoA carboxylase (ACC), lipin-1, adipose tissue
triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), were analyzed
in the VAT of treated rats. Tissue inflammationevaluated by nuclear
factor kappa B (NFκB)protein level and intracellular distribution, as well as
by TNFα, IL6 and IL1β mRNA levels. Glucocorticoid signaling was examined
at the level of 11 beta hydroxysteroid dehydrogenase type 1 (11βHSD1)
and 5α-reductase, as well asby glucocorticoid receptor (GR) leveland its
subcellular distribution. The results showed that DHT treatment induced increase
of lipogenic factors (SREBP-1, lipin-1, FAS and PEPCK), while the
level of lipolytic enzyme HSL was decreasedin VAT. These molecular alterations
were accompanied by adipocyte hypertrophy, visceral obesity and
elevated plasma FFA and triglyceride concentrations. Those changes in lipid
metabolism were possible trigger for low-grade inflammation observed in
the VAT and characterized by NFκB activation and increasedIL6 and IL1β
mRNA levels. In spite of increased VAT proinflammatory mediators, the
level of proinflammatory cytokines, IL6 and IL1β, was decreased in the liver
of DHT-treated rats, while the activation of NFκB remained unchanged.
The state of suppressed inflammation in the liver could be an outcome of
stimulated glucocorticoid signaling, as judged byincreased hepatic corticosterone
level and GR activation. The augmentation of hepatic glucocorticoids
could be a net result of increased expression of 11βHSD1 and decreased
expression of 5β-reductase mRNA. In conclusion, the results showed that
abdominal obesity and dyslipidemia in the animal model of PCOS were accompanied
with hypertrophic adipocytes, lipid accumulation and low-grade
inflammation in the VAT. However, these metabolic disturbances did not resultin
hepatic inflammation due to increased tissue levels of glucocorticoids.",
publisher = "European Society of Endocrinology",
journal = "22nd European Congress of Endocrinology: Abstracts; 2020 Sep 5-9",
title = "Different effects of 5α-dihydrotestosterone treatment on hepatic and visceral adipose tissue inflammation in animal model of polycystic ovary syndrome",
doi = "10.1530/endoabs.70.AEP382",
pages = "AEP382"
}

Vojnović-Milutinović, D., Veličković, N., Radovanović, M., Đorđević, A., Brkljačić, J., Teofilović, A., Bursać, B., Jelača, S.,& Macut, Đ.. (2020). Different effects of 5α-dihydrotestosterone treatment on hepatic and visceral adipose tissue inflammation in animal model of polycystic ovary syndrome. in 22nd European Congress of Endocrinology: Abstracts; 2020 Sep 5-9
European Society of Endocrinology., AEP382.
https://doi.org/10.1530/endoabs.70.AEP382

Vojnović-Milutinović D, Veličković N, Radovanović M, Đorđević A, Brkljačić J, Teofilović A, Bursać B, Jelača S, Macut Đ. Different effects of 5α-dihydrotestosterone treatment on hepatic and visceral adipose tissue inflammation in animal model of polycystic ovary syndrome. in 22nd European Congress of Endocrinology: Abstracts; 2020 Sep 5-9. 2020;:AEP382.
doi:10.1530/endoabs.70.AEP382 .

Vojnović-Milutinović, Danijela, Veličković, Nataša, Radovanović, Marina, Đorđević, Ana, Brkljačić, Jelena, Teofilović, Ana, Bursać, Biljana, Jelača, Sanja, Macut, Đuro, "Different effects of 5α-dihydrotestosterone treatment on hepatic and visceral adipose tissue inflammation in animal model of polycystic ovary syndrome" in 22nd European Congress of Endocrinology: Abstracts; 2020 Sep 5-9 (2020):AEP382,
https://doi.org/10.1530/endoabs.70.AEP382 . .

TY  - CONF
AU  - Radovanović, Marina
AU  - Kovačević, Sanja
AU  - Elaković, Ivana
AU  - Vojnović-Milutinović, Danijela
AU  - Matić, Gordana
AU  - Brkljačić, Jelena
PY  - 2019
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5252
AB  - The effects of early-life fructose consumption and their relation to metabolic diseases risk
in adulthood are not yet elucidated. This study explored the direct effects of a diet regime
characterized by fructose enrichment on glucocorticoid receptor signaling in the liver of
female rats immediately after weaning. 21 day-old female Wistar rats were subjected to a 9
week-long diet regime involving standard chow in combination with either the 10%
fructose solution or tap water. Glucocorticoid receptor hormone binding parameters,
intracellular distribution of this molecule as well as the expression of its target genes
involved in lipid metabolism (most notably Lipin-1) and glucose metabolism (PEPCK),
were measured. An increase in the hepatic glucocorticoid receptor hormone binding
activity as well as an elevated nuclear translocation of the receptor, in concert with the
increased protein levels of Lipin-1 were observed after fructose enriched diet. This was
preceeded by a hepatic elevation in Glut-2 fructose transporter expression. Fructose-
enriched diet starting immediately after weaning enhanced hepatic glucocorticoid signaling
in young female rats and promoted lypogenesis as evidenced not only by the lipin-1
increase but also by FAS, ACC and SCREBP-1 expression elevations contributing to
hypertriglyceridemia and the expansion of the visceral adipose tissue 1, with no effect on
the hepatic gluconeogenesis. These results imply that while most parameters remained
within physiological reactivity, prolonged treatment might ultimately lead to more
pronounced metabolic disturbances.
PB  - Belgrade: Faculty of Chemistry
C3  - The 9th Conference of the Serbian Biochemical Society: Diversity in Biochemistry; 2019 Nov 14-16; Belgrade, Serbia
T1  - Fructose consumption affects glucocorticoid receptor signaling and increases lipogenesis in the liver of young female rats
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5252
ER  - 

@conference{
author = "Radovanović, Marina and Kovačević, Sanja and Elaković, Ivana and Vojnović-Milutinović, Danijela and Matić, Gordana and Brkljačić, Jelena",
year = "2019",
abstract = "The effects of early-life fructose consumption and their relation to metabolic diseases risk
in adulthood are not yet elucidated. This study explored the direct effects of a diet regime
characterized by fructose enrichment on glucocorticoid receptor signaling in the liver of
female rats immediately after weaning. 21 day-old female Wistar rats were subjected to a 9
week-long diet regime involving standard chow in combination with either the 10%
fructose solution or tap water. Glucocorticoid receptor hormone binding parameters,
intracellular distribution of this molecule as well as the expression of its target genes
involved in lipid metabolism (most notably Lipin-1) and glucose metabolism (PEPCK),
were measured. An increase in the hepatic glucocorticoid receptor hormone binding
activity as well as an elevated nuclear translocation of the receptor, in concert with the
increased protein levels of Lipin-1 were observed after fructose enriched diet. This was
preceeded by a hepatic elevation in Glut-2 fructose transporter expression. Fructose-
enriched diet starting immediately after weaning enhanced hepatic glucocorticoid signaling
in young female rats and promoted lypogenesis as evidenced not only by the lipin-1
increase but also by FAS, ACC and SCREBP-1 expression elevations contributing to
hypertriglyceridemia and the expansion of the visceral adipose tissue 1, with no effect on
the hepatic gluconeogenesis. These results imply that while most parameters remained
within physiological reactivity, prolonged treatment might ultimately lead to more
pronounced metabolic disturbances.",
publisher = "Belgrade: Faculty of Chemistry",
journal = "The 9th Conference of the Serbian Biochemical Society: Diversity in Biochemistry; 2019 Nov 14-16; Belgrade, Serbia",
title = "Fructose consumption affects glucocorticoid receptor signaling and increases lipogenesis in the liver of young female rats",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5252"
}

Radovanović, M., Kovačević, S., Elaković, I., Vojnović-Milutinović, D., Matić, G.,& Brkljačić, J.. (2019). Fructose consumption affects glucocorticoid receptor signaling and increases lipogenesis in the liver of young female rats. in The 9th Conference of the Serbian Biochemical Society: Diversity in Biochemistry; 2019 Nov 14-16; Belgrade, Serbia
Belgrade: Faculty of Chemistry..
https://hdl.handle.net/21.15107/rcub_ibiss_5252

Radovanović M, Kovačević S, Elaković I, Vojnović-Milutinović D, Matić G, Brkljačić J. Fructose consumption affects glucocorticoid receptor signaling and increases lipogenesis in the liver of young female rats. in The 9th Conference of the Serbian Biochemical Society: Diversity in Biochemistry; 2019 Nov 14-16; Belgrade, Serbia. 2019;.
https://hdl.handle.net/21.15107/rcub_ibiss_5252 .

Radovanović, Marina, Kovačević, Sanja, Elaković, Ivana, Vojnović-Milutinović, Danijela, Matić, Gordana, Brkljačić, Jelena, "Fructose consumption affects glucocorticoid receptor signaling and increases lipogenesis in the liver of young female rats" in The 9th Conference of the Serbian Biochemical Society: Diversity in Biochemistry; 2019 Nov 14-16; Belgrade, Serbia (2019),
https://hdl.handle.net/21.15107/rcub_ibiss_5252 .

TY  - CONF
AU  - Veličković, Nataša
AU  - Vojnović-Milutinović, Danijela
AU  - Brkljačić, Jelena
AU  - Teofilović, Ana
AU  - Bursać, Biljana
AU  - Radovanović, Marina
AU  - Gligorovska, Ljupka
AU  - Kovačević, Sanja
AU  - Matić, Gordana
AU  - Đorđević, Ana
PY  - 2019
UR  - https://www.isos.rs/congress-2019
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3991
AB  - Fructose overconsumption, especially in the form of sweetened beverages, has been linked to development of obesity, insulin resistance, dyslipidemia and type 2 diabetes. In rodents, high-fructose diet leads to hypertriglyceridemia, ectopic fat deposition and insulin resistance. Metabolically triggered inflammation (metaflammation) is now recognized as a link between nutrient signals and insulin resistance and considered as usual suspect for metabolic disturbances. Metaflammation usually evolve from visceral adipose tissue, progresses to liver and brain strucures, and results in peripheral insulin resistance, lipid accumulation and oxidative stress. Hence, the aim of our study was to investigate metaflammation as a trigger for fructose-induced metabolic disturbances. Experiments were performed on male Wistar rats fed with different concentrations of liquid fructose (10, 20 and 60%) during 9 weeks. Physiological and biochemical parameters, hepatic and brain inflammation, indicators of peripheral and systemic insulin resistance, as well as hepatic lipogenesis and oxidative stress were examined. The results demonstrated that fructose-enriched diet generally led to increased proinflamatory cytokines in the liver, hippocampus and hypothalamus, and to stimulated activation of proinflamatory kinases NFκB and JNK, while it did not change the expression of inflammasome component NLRP3, toll-like receptor 4 or anti-inflammatory cytokines in the liver. The observed metabolic inflammation was accompanied with impaired glucose tolerance after 10 and 20% fructose-enriched diet, while decreased hepatic insulin sensitivity, hypetriglyceridemia and increased expression of hepatic lipogenic genes were observed after all fructose diets. The treatment of fructose-fed rats with chronic unpredictable stress annulled the effects of fructose on hepatic and hypothalamic inflammation and glucose tolerance, but did not alter fructose-induced effects on lipogenesis and insulin signaling. The results suggest that fructose-induced metaflammation and systemic insulin resistance are closely interconnected, while the link between inflammation and other metabolic disturbances could still be a matter of debate.
PB  - Institute for Biological Research "Siniša Stanković" - National Institute of Republic of Serbia, University of Belgrade
PB  - Immunological Society of Serbia
C3  - Immunology at the Confluence of Multidisciplinary Approaches : abstract book
T1  - Is Metaflammation a Usual Suspect for Fructose-induced Metabolic Disturbances?
SP  - 51
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_3991
ER  - 

@conference{
author = "Veličković, Nataša and Vojnović-Milutinović, Danijela and Brkljačić, Jelena and Teofilović, Ana and Bursać, Biljana and Radovanović, Marina and Gligorovska, Ljupka and Kovačević, Sanja and Matić, Gordana and Đorđević, Ana",
year = "2019",
abstract = "Fructose overconsumption, especially in the form of sweetened beverages, has been linked to development of obesity, insulin resistance, dyslipidemia and type 2 diabetes. In rodents, high-fructose diet leads to hypertriglyceridemia, ectopic fat deposition and insulin resistance. Metabolically triggered inflammation (metaflammation) is now recognized as a link between nutrient signals and insulin resistance and considered as usual suspect for metabolic disturbances. Metaflammation usually evolve from visceral adipose tissue, progresses to liver and brain strucures, and results in peripheral insulin resistance, lipid accumulation and oxidative stress. Hence, the aim of our study was to investigate metaflammation as a trigger for fructose-induced metabolic disturbances. Experiments were performed on male Wistar rats fed with different concentrations of liquid fructose (10, 20 and 60%) during 9 weeks. Physiological and biochemical parameters, hepatic and brain inflammation, indicators of peripheral and systemic insulin resistance, as well as hepatic lipogenesis and oxidative stress were examined. The results demonstrated that fructose-enriched diet generally led to increased proinflamatory cytokines in the liver, hippocampus and hypothalamus, and to stimulated activation of proinflamatory kinases NFκB and JNK, while it did not change the expression of inflammasome component NLRP3, toll-like receptor 4 or anti-inflammatory cytokines in the liver. The observed metabolic inflammation was accompanied with impaired glucose tolerance after 10 and 20% fructose-enriched diet, while decreased hepatic insulin sensitivity, hypetriglyceridemia and increased expression of hepatic lipogenic genes were observed after all fructose diets. The treatment of fructose-fed rats with chronic unpredictable stress annulled the effects of fructose on hepatic and hypothalamic inflammation and glucose tolerance, but did not alter fructose-induced effects on lipogenesis and insulin signaling. The results suggest that fructose-induced metaflammation and systemic insulin resistance are closely interconnected, while the link between inflammation and other metabolic disturbances could still be a matter of debate.",
publisher = "Institute for Biological Research "Siniša Stanković" - National Institute of Republic of Serbia, University of Belgrade, Immunological Society of Serbia",
journal = "Immunology at the Confluence of Multidisciplinary Approaches : abstract book",
title = "Is Metaflammation a Usual Suspect for Fructose-induced Metabolic Disturbances?",
pages = "51",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_3991"
}

Veličković, N., Vojnović-Milutinović, D., Brkljačić, J., Teofilović, A., Bursać, B., Radovanović, M., Gligorovska, L., Kovačević, S., Matić, G.,& Đorđević, A.. (2019). Is Metaflammation a Usual Suspect for Fructose-induced Metabolic Disturbances?. in Immunology at the Confluence of Multidisciplinary Approaches : abstract book
Institute for Biological Research "Siniša Stanković" - National Institute of Republic of Serbia, University of Belgrade., 51.
https://hdl.handle.net/21.15107/rcub_ibiss_3991

Veličković N, Vojnović-Milutinović D, Brkljačić J, Teofilović A, Bursać B, Radovanović M, Gligorovska L, Kovačević S, Matić G, Đorđević A. Is Metaflammation a Usual Suspect for Fructose-induced Metabolic Disturbances?. in Immunology at the Confluence of Multidisciplinary Approaches : abstract book. 2019;:51.
https://hdl.handle.net/21.15107/rcub_ibiss_3991 .

Veličković, Nataša, Vojnović-Milutinović, Danijela, Brkljačić, Jelena, Teofilović, Ana, Bursać, Biljana, Radovanović, Marina, Gligorovska, Ljupka, Kovačević, Sanja, Matić, Gordana, Đorđević, Ana, "Is Metaflammation a Usual Suspect for Fructose-induced Metabolic Disturbances?" in Immunology at the Confluence of Multidisciplinary Approaches : abstract book (2019):51,
https://hdl.handle.net/21.15107/rcub_ibiss_3991 .

TY  - CONF
AU  - Veličković, Nataša
AU  - Teofilović, Ana
AU  - Đorđević, Ana
AU  - Vojnović-Milutinović, Danijela
AU  - Bursać, Biljana
AU  - Brkljačić, Jelena
AU  - Elaković, Ivana
AU  - Kovačević, Sanja
AU  - Gligorovska, Ljupka
AU  - Radovanović, Marina
AU  - Preitner, Frederic
AU  - Tappy, Luc
AU  - Matić, Gordana
PY  - 2018
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5253
AB  - The aim: High fructose diet and chronic stress were both
linked with metabolic disturbances. Thus, we analyzed
their separate and combined effects on metabolic ho-
meostasis, with particular focus on hepatic lipogenesis
and gluconeogenesis.
Methods: Male Wistar rats were subjected to 9-week
20% fructose diet and/or 4-week chronic unpredict-
able stress. The following morphological and bio-
chemical parameters of lipid and glucose metabolism
were measured: body and liver mass, energy intake,
blood glucose and plasma insulin levels, free fatty ac-
ids (FFA), lactate, triglycerides (TG) and VLDL-TG, as
well as hepatic VLDL production rate, total hepatic TG
and palmitate and stearate percentage shares. Fur-
thermore, the expression of transcriptional regulators
and enzymes of hepatic de novo lipogenesis (DNL), li-
poprotein export and gluconeogenesis were analyzed.
Results: Although energy intake was increased after
fructose diet, body and liver mass remained unaltered.
Plasma TG were elevated in both fructose-fed groups,
whereas FFA were increased in the non-stressed fruc-
tose-fed group. Parameters of hepatic TG and VLDL
production and export were unaffected, except for the
hepatic palmitate production which was increased after
combined treatment. The increments of fractional DNL
and palmitate production accompanied the upregu-
lation of lipogenic enzymes, fatty acid sythase and
acetyl-CoA carboxylase, which was, interestingly, not
preceeded by the increase of their transcriptional reg-
ulators. In both fructose-fed groups blood glucose level
was increased, although hepatic gluconeogenesis
was unaffected.
Conclusion: Combined stress/fructose treatment is
more aggravating than separate treatments, since it
leads to an increase in hepatic de novo lipogenesis
and total hepatic TG palmitate, without concomitant
changes in VLDL production and export.
PB  - Belgrade: Institute for Biological Research "Siniša Stanković"– National Institute of Republic of Serbia, University of Belgrade
C3  - Program & Book of Abstracts: IUBMB Advanced School Nutrition, Metabolism and Aging; 2018 Oct 15-19; Petnica, Serbia.
T1  - De novo lipogenesis and gluconeogenesis in the liver of male fructose-fed rats exposed to chronic stress
SP  - 18
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5253
ER  - 

@conference{
author = "Veličković, Nataša and Teofilović, Ana and Đorđević, Ana and Vojnović-Milutinović, Danijela and Bursać, Biljana and Brkljačić, Jelena and Elaković, Ivana and Kovačević, Sanja and Gligorovska, Ljupka and Radovanović, Marina and Preitner, Frederic and Tappy, Luc and Matić, Gordana",
year = "2018",
abstract = "The aim: High fructose diet and chronic stress were both
linked with metabolic disturbances. Thus, we analyzed
their separate and combined effects on metabolic ho-
meostasis, with particular focus on hepatic lipogenesis
and gluconeogenesis.
Methods: Male Wistar rats were subjected to 9-week
20% fructose diet and/or 4-week chronic unpredict-
able stress. The following morphological and bio-
chemical parameters of lipid and glucose metabolism
were measured: body and liver mass, energy intake,
blood glucose and plasma insulin levels, free fatty ac-
ids (FFA), lactate, triglycerides (TG) and VLDL-TG, as
well as hepatic VLDL production rate, total hepatic TG
and palmitate and stearate percentage shares. Fur-
thermore, the expression of transcriptional regulators
and enzymes of hepatic de novo lipogenesis (DNL), li-
poprotein export and gluconeogenesis were analyzed.
Results: Although energy intake was increased after
fructose diet, body and liver mass remained unaltered.
Plasma TG were elevated in both fructose-fed groups,
whereas FFA were increased in the non-stressed fruc-
tose-fed group. Parameters of hepatic TG and VLDL
production and export were unaffected, except for the
hepatic palmitate production which was increased after
combined treatment. The increments of fractional DNL
and palmitate production accompanied the upregu-
lation of lipogenic enzymes, fatty acid sythase and
acetyl-CoA carboxylase, which was, interestingly, not
preceeded by the increase of their transcriptional reg-
ulators. In both fructose-fed groups blood glucose level
was increased, although hepatic gluconeogenesis
was unaffected.
Conclusion: Combined stress/fructose treatment is
more aggravating than separate treatments, since it
leads to an increase in hepatic de novo lipogenesis
and total hepatic TG palmitate, without concomitant
changes in VLDL production and export.",
publisher = "Belgrade: Institute for Biological Research "Siniša Stanković"– National Institute of Republic of Serbia, University of Belgrade",
journal = "Program & Book of Abstracts: IUBMB Advanced School Nutrition, Metabolism and Aging; 2018 Oct 15-19; Petnica, Serbia.",
title = "De novo lipogenesis and gluconeogenesis in the liver of male fructose-fed rats exposed to chronic stress",
pages = "18",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5253"
}

Veličković, N., Teofilović, A., Đorđević, A., Vojnović-Milutinović, D., Bursać, B., Brkljačić, J., Elaković, I., Kovačević, S., Gligorovska, L., Radovanović, M., Preitner, F., Tappy, L.,& Matić, G.. (2018). De novo lipogenesis and gluconeogenesis in the liver of male fructose-fed rats exposed to chronic stress. in Program & Book of Abstracts: IUBMB Advanced School Nutrition, Metabolism and Aging; 2018 Oct 15-19; Petnica, Serbia.
Belgrade: Institute for Biological Research "Siniša Stanković"– National Institute of Republic of Serbia, University of Belgrade., 18.
https://hdl.handle.net/21.15107/rcub_ibiss_5253

Veličković N, Teofilović A, Đorđević A, Vojnović-Milutinović D, Bursać B, Brkljačić J, Elaković I, Kovačević S, Gligorovska L, Radovanović M, Preitner F, Tappy L, Matić G. De novo lipogenesis and gluconeogenesis in the liver of male fructose-fed rats exposed to chronic stress. in Program & Book of Abstracts: IUBMB Advanced School Nutrition, Metabolism and Aging; 2018 Oct 15-19; Petnica, Serbia.. 2018;:18.
https://hdl.handle.net/21.15107/rcub_ibiss_5253 .

Veličković, Nataša, Teofilović, Ana, Đorđević, Ana, Vojnović-Milutinović, Danijela, Bursać, Biljana, Brkljačić, Jelena, Elaković, Ivana, Kovačević, Sanja, Gligorovska, Ljupka, Radovanović, Marina, Preitner, Frederic, Tappy, Luc, Matić, Gordana, "De novo lipogenesis and gluconeogenesis in the liver of male fructose-fed rats exposed to chronic stress" in Program & Book of Abstracts: IUBMB Advanced School Nutrition, Metabolism and Aging; 2018 Oct 15-19; Petnica, Serbia. (2018):18,
https://hdl.handle.net/21.15107/rcub_ibiss_5253 .

TY  - JOUR
AU  - Vojnović Milutinović, Danijela
AU  - Radovanović, Marina
AU  - Veličković, Nataša
AU  - Đorđević, Ana
AU  - Bursać, Biljana
AU  - Brkljačić, Jelena
AU  - Teofilović, Ana
AU  - Božić Antić, Ivana
AU  - Bjekić-Macut, Jelica
AU  - Shirif Zidane, Abdulbaset
AU  - Matić, Gordana
AU  - Macut, Đuro
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6331
AB  - Polycystic ovary syndrome is a heterogeneous endocrine and metabolic disorder associated with abdominal obesity, dyslipidemia and insulin resistance. Since abdominal obesity is characterized by low-grade inflammation, the aim of the study was to investigate whether visceral adipose tissue inflammation linked to abdominal obesity and dyslipidemia could lead to impaired insulin sensitivity in the animal model of polycystic ovary syndrome. 
Female Wistar rats were treated with nonaromatizable 5α dihydrotestosterone pellets in order to induce reproductive and metabolic characteristics of polycystic ovary syndrome. Glucose, triglycerides, non-esterified fatty acids and insulin were determined in blood plasma. Visceral adipose tissue inflammation was evaluated by the nuclear factor kappa B intracellular distribution, macrophage migration inhibitory factor protein level, as well as TNFα, IL6 and IL1β mRNA levels. Insulin sensitivity was assessed by intraperitoneal glucose tolerance test and homeostasis model assessment index, and through analysis of insulin signaling pathway in the visceral adipose tissue.
Dihydrotestosterone treatment led to increased body weight, abdominal obesity and elevated triglycerides and non-esterified fatty acids, which were accompanied by the activation of nuclear factor kappa B and increase in macrophage migration inhibitory factor, IL6 and IL1β levels in the visceral adipose tissue. In parallel, insulin sensitivity was affected in 5α dihydrotestosterone-treated animals only at the systemic, and not at the level of visceral adipose tissue. 
The results showed that abdominal obesity and dyslipidemia in the animal model of polycystic ovary syndrome were accompanied with low-grade inflammation in the visceral adipose tissue. However, these metabolic disturbances did not result in decreased tissue insulin sensitivity.
PB  - Stuttgart: Georg Thieme Verlag KG
T2  - Experimental and Clinical Endocrinology and Diabetes
T1  - Enhanced inflammation without impairment of insulin signaling in the visceral adipose tissue of 5α- dihydrotestosterone-induced animal model of polycystic ovary syndrome
IS  - 8
VL  - 125
DO  - 10.1055/s-0043-104531
SP  - 522
EP  - 529
ER  - 

@article{
author = "Vojnović Milutinović, Danijela and Radovanović, Marina and Veličković, Nataša and Đorđević, Ana and Bursać, Biljana and Brkljačić, Jelena and Teofilović, Ana and Božić Antić, Ivana and Bjekić-Macut, Jelica and Shirif Zidane, Abdulbaset and Matić, Gordana and Macut, Đuro",
year = "2017",
abstract = "Polycystic ovary syndrome is a heterogeneous endocrine and metabolic disorder associated with abdominal obesity, dyslipidemia and insulin resistance. Since abdominal obesity is characterized by low-grade inflammation, the aim of the study was to investigate whether visceral adipose tissue inflammation linked to abdominal obesity and dyslipidemia could lead to impaired insulin sensitivity in the animal model of polycystic ovary syndrome. 
Female Wistar rats were treated with nonaromatizable 5α dihydrotestosterone pellets in order to induce reproductive and metabolic characteristics of polycystic ovary syndrome. Glucose, triglycerides, non-esterified fatty acids and insulin were determined in blood plasma. Visceral adipose tissue inflammation was evaluated by the nuclear factor kappa B intracellular distribution, macrophage migration inhibitory factor protein level, as well as TNFα, IL6 and IL1β mRNA levels. Insulin sensitivity was assessed by intraperitoneal glucose tolerance test and homeostasis model assessment index, and through analysis of insulin signaling pathway in the visceral adipose tissue.
Dihydrotestosterone treatment led to increased body weight, abdominal obesity and elevated triglycerides and non-esterified fatty acids, which were accompanied by the activation of nuclear factor kappa B and increase in macrophage migration inhibitory factor, IL6 and IL1β levels in the visceral adipose tissue. In parallel, insulin sensitivity was affected in 5α dihydrotestosterone-treated animals only at the systemic, and not at the level of visceral adipose tissue. 
The results showed that abdominal obesity and dyslipidemia in the animal model of polycystic ovary syndrome were accompanied with low-grade inflammation in the visceral adipose tissue. However, these metabolic disturbances did not result in decreased tissue insulin sensitivity.",
publisher = "Stuttgart: Georg Thieme Verlag KG",
journal = "Experimental and Clinical Endocrinology and Diabetes",
title = "Enhanced inflammation without impairment of insulin signaling in the visceral adipose tissue of 5α- dihydrotestosterone-induced animal model of polycystic ovary syndrome",
number = "8",
volume = "125",
doi = "10.1055/s-0043-104531",
pages = "522-529"
}

Vojnović Milutinović, D., Radovanović, M., Veličković, N., Đorđević, A., Bursać, B., Brkljačić, J., Teofilović, A., Božić Antić, I., Bjekić-Macut, J., Shirif Zidane, A., Matić, G.,& Macut, Đ.. (2017). Enhanced inflammation without impairment of insulin signaling in the visceral adipose tissue of 5α- dihydrotestosterone-induced animal model of polycystic ovary syndrome. in Experimental and Clinical Endocrinology and Diabetes
Stuttgart: Georg Thieme Verlag KG., 125(8), 522-529.
https://doi.org/10.1055/s-0043-104531

Vojnović Milutinović D, Radovanović M, Veličković N, Đorđević A, Bursać B, Brkljačić J, Teofilović A, Božić Antić I, Bjekić-Macut J, Shirif Zidane A, Matić G, Macut Đ. Enhanced inflammation without impairment of insulin signaling in the visceral adipose tissue of 5α- dihydrotestosterone-induced animal model of polycystic ovary syndrome. in Experimental and Clinical Endocrinology and Diabetes. 2017;125(8):522-529.
doi:10.1055/s-0043-104531 .

Vojnović Milutinović, Danijela, Radovanović, Marina, Veličković, Nataša, Đorđević, Ana, Bursać, Biljana, Brkljačić, Jelena, Teofilović, Ana, Božić Antić, Ivana, Bjekić-Macut, Jelica, Shirif Zidane, Abdulbaset, Matić, Gordana, Macut, Đuro, "Enhanced inflammation without impairment of insulin signaling in the visceral adipose tissue of 5α- dihydrotestosterone-induced animal model of polycystic ovary syndrome" in Experimental and Clinical Endocrinology and Diabetes, 125, no. 8 (2017):522-529,
https://doi.org/10.1055/s-0043-104531 . .

TY  - CONF
AU  - Jelača, Sanja
AU  - Brkljačić, Jelena
AU  - Veličković, Nataša
AU  - Teofilović, Ana
AU  - Đorđević, Ana
AU  - Radovanović, Marina
AU  - Macut, Đuro
AU  - Božić-Antić, Ivana
AU  - Matić, Gordana
AU  - Vojnović-Milutinović, Danijela
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5518
AB  - Introduction: Polycystic ovary syndrome (PCOS) is a reproductive and metabolic disorder characterized by hyperandrogenism, ovulatory dysfunction, visceral obesity and insulin resistance. PCOS is also associated with enhanced cortisol metabolite excretion, as well as with altered peripheral glucocorticoid metabolism, which is inevitably linked to insulin resistance characteristic for women with PCOS. The main enzymes involved in glucocorticoid prereceptor metabolism are 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1) that regenerates corticosterone from its inactive precursor, and 5α and 5β reductases (5αR and 5βR) that inactivate corticosterone. In this study, female rats treated with nonaromatizable 5α-dihydrotestosterone (DHT) were used as an animal model of PCOS and the aim was to examine whether this treatment affects hepatic glucocorticoid prereceptor metabolism.
Methods: We analyzed the effects of prolonged treatment of prepubertal rats with DHT on body and liver masses, and plasma and liver corticosterone levels. The expression of hepatic 11βHSD1, hexose-6-phosphate dehydrogenase (H6PDH), 5αR, 5βR and glucocorticoid receptor (GR) were analyzed by real-time PCR and Western blot methods.
Results: DHT treatment induced an increase in body and liver masses, an elevation of hepatic 11βHSD1 expression and a reduction of 5αR mRNA level, leading to tissue corticosterone rise and GR nuclear accumulation. In addition, H6PDH and 5βR mRNA levels remained unchanged.
Conclusion: DHT treatment affected hepatic glucocorticoid prereceptor metabolism through enhanced corticosterone availability and its decreased inactivation, which led to enhanced GR activation. Further studies should reveal possible link between enhanced hepatic glucocorticoid signaling and metabolic disturbances observed in PCOS.
PB  - Belgrade: University of Belgrade, Faculty of Biology
C3  - CoMBoS. Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia
T1  - Glucocorticoid prereceptor metabolism in the liver of 5α-dihidrotestosterone-treated rats as animal model of polycystic ovary syndrome
SP  - 42
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5518
ER  - 

@conference{
author = "Jelača, Sanja and Brkljačić, Jelena and Veličković, Nataša and Teofilović, Ana and Đorđević, Ana and Radovanović, Marina and Macut, Đuro and Božić-Antić, Ivana and Matić, Gordana and Vojnović-Milutinović, Danijela",
year = "2017",
abstract = "Introduction: Polycystic ovary syndrome (PCOS) is a reproductive and metabolic disorder characterized by hyperandrogenism, ovulatory dysfunction, visceral obesity and insulin resistance. PCOS is also associated with enhanced cortisol metabolite excretion, as well as with altered peripheral glucocorticoid metabolism, which is inevitably linked to insulin resistance characteristic for women with PCOS. The main enzymes involved in glucocorticoid prereceptor metabolism are 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1) that regenerates corticosterone from its inactive precursor, and 5α and 5β reductases (5αR and 5βR) that inactivate corticosterone. In this study, female rats treated with nonaromatizable 5α-dihydrotestosterone (DHT) were used as an animal model of PCOS and the aim was to examine whether this treatment affects hepatic glucocorticoid prereceptor metabolism.
Methods: We analyzed the effects of prolonged treatment of prepubertal rats with DHT on body and liver masses, and plasma and liver corticosterone levels. The expression of hepatic 11βHSD1, hexose-6-phosphate dehydrogenase (H6PDH), 5αR, 5βR and glucocorticoid receptor (GR) were analyzed by real-time PCR and Western blot methods.
Results: DHT treatment induced an increase in body and liver masses, an elevation of hepatic 11βHSD1 expression and a reduction of 5αR mRNA level, leading to tissue corticosterone rise and GR nuclear accumulation. In addition, H6PDH and 5βR mRNA levels remained unchanged.
Conclusion: DHT treatment affected hepatic glucocorticoid prereceptor metabolism through enhanced corticosterone availability and its decreased inactivation, which led to enhanced GR activation. Further studies should reveal possible link between enhanced hepatic glucocorticoid signaling and metabolic disturbances observed in PCOS.",
publisher = "Belgrade: University of Belgrade, Faculty of Biology",
journal = "CoMBoS. Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia",
title = "Glucocorticoid prereceptor metabolism in the liver of 5α-dihidrotestosterone-treated rats as animal model of polycystic ovary syndrome",
pages = "42",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5518"
}

Jelača, S., Brkljačić, J., Veličković, N., Teofilović, A., Đorđević, A., Radovanović, M., Macut, Đ., Božić-Antić, I., Matić, G.,& Vojnović-Milutinović, D.. (2017). Glucocorticoid prereceptor metabolism in the liver of 5α-dihidrotestosterone-treated rats as animal model of polycystic ovary syndrome. in CoMBoS. Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia
Belgrade: University of Belgrade, Faculty of Biology., 42.
https://hdl.handle.net/21.15107/rcub_ibiss_5518

Jelača S, Brkljačić J, Veličković N, Teofilović A, Đorđević A, Radovanović M, Macut Đ, Božić-Antić I, Matić G, Vojnović-Milutinović D. Glucocorticoid prereceptor metabolism in the liver of 5α-dihidrotestosterone-treated rats as animal model of polycystic ovary syndrome. in CoMBoS. Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia. 2017;:42.
https://hdl.handle.net/21.15107/rcub_ibiss_5518 .

Jelača, Sanja, Brkljačić, Jelena, Veličković, Nataša, Teofilović, Ana, Đorđević, Ana, Radovanović, Marina, Macut, Đuro, Božić-Antić, Ivana, Matić, Gordana, Vojnović-Milutinović, Danijela, "Glucocorticoid prereceptor metabolism in the liver of 5α-dihidrotestosterone-treated rats as animal model of polycystic ovary syndrome" in CoMBoS. Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia (2017):42,
https://hdl.handle.net/21.15107/rcub_ibiss_5518 .

TY  - JOUR
AU  - Radovanović, Marina
AU  - Veličković, Nataša
AU  - Đorđević, Ana
AU  - Bursać, Biljana
AU  - Macut, Đuro
AU  - Božić Antić, Ivana
AU  - Bjekić Macut, Jelica
AU  - Matić, Gordana
AU  - Vojnović-Milutinović, Danijela
PY  - 2016
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6151
AB  - Polycystic ovary syndrome (PCOS) is the most common endocrinopathy in women of reproductive age. It is a
heterogenous disorder, with hyperandrogenism, chronic anovulation and polycystic ovaries as basic characteristics, and
associated metabolic syndrome features. Increased secretion of leptin and leptin resistance are common consequences
of obesity. Leptin is a hormone with anorexigenic effects in the hypothalamus. Its function in the regulation of energy
intake and consumption is antagonized by glucocorticoids. By modulating leptin signaling and inflammatory processes in
the hypothalamus, glucocorticoids can contribute to the development of metabolic disturbances associated with central
energy disbalance. The aim of the study was to examine the relationship between hypothalamic leptin, glucocorticoid and
inflammatory signaling in the development of metabolic disturbances associated with PCOS. The study was conducted on
an animal model of PCOS generated by a continual, 90-day treatment of female rats with 5α-dihydrotestosterone (DHT).
The model exhibited all key reproductive and metabolic features of the syndrome. mRNA and/or protein levels of the key
components of hypothalamic glucocorticoid, leptin and inflammatory pathways, presumably contributing to energy disbalance
in DHT-treated female rats, were measured. The results indicated that DHT treatment led to the development of
hyperphagia and hyperleptinemia as metabolic features associated with PCOS. However, these metabolic disturbances could
not be ascribed to changes in hypothalamic leptin, glucocorticoid or inflammatory signaling pathways in DHT-treated rats.
PB  - Belgrrade: Serbian Biological Society
T2  - Archives of Biological Sciences
T1  - 5α-dihydrotestosterone treatment induces metabolic changes associated with Polycystic ovary syndrome without interfering with hypothalamic leptin and glucocorticoid signaling
IS  - 3
VL  - 68
DO  - 10.2298/ABS151214001N
SP  - 473
EP  - 481
ER  - 

@article{
author = "Radovanović, Marina and Veličković, Nataša and Đorđević, Ana and Bursać, Biljana and Macut, Đuro and Božić Antić, Ivana and Bjekić Macut, Jelica and Matić, Gordana and Vojnović-Milutinović, Danijela",
year = "2016",
abstract = "Polycystic ovary syndrome (PCOS) is the most common endocrinopathy in women of reproductive age. It is a
heterogenous disorder, with hyperandrogenism, chronic anovulation and polycystic ovaries as basic characteristics, and
associated metabolic syndrome features. Increased secretion of leptin and leptin resistance are common consequences
of obesity. Leptin is a hormone with anorexigenic effects in the hypothalamus. Its function in the regulation of energy
intake and consumption is antagonized by glucocorticoids. By modulating leptin signaling and inflammatory processes in
the hypothalamus, glucocorticoids can contribute to the development of metabolic disturbances associated with central
energy disbalance. The aim of the study was to examine the relationship between hypothalamic leptin, glucocorticoid and
inflammatory signaling in the development of metabolic disturbances associated with PCOS. The study was conducted on
an animal model of PCOS generated by a continual, 90-day treatment of female rats with 5α-dihydrotestosterone (DHT).
The model exhibited all key reproductive and metabolic features of the syndrome. mRNA and/or protein levels of the key
components of hypothalamic glucocorticoid, leptin and inflammatory pathways, presumably contributing to energy disbalance
in DHT-treated female rats, were measured. The results indicated that DHT treatment led to the development of
hyperphagia and hyperleptinemia as metabolic features associated with PCOS. However, these metabolic disturbances could
not be ascribed to changes in hypothalamic leptin, glucocorticoid or inflammatory signaling pathways in DHT-treated rats.",
publisher = "Belgrrade: Serbian Biological Society",
journal = "Archives of Biological Sciences",
title = "5α-dihydrotestosterone treatment induces metabolic changes associated with Polycystic ovary syndrome without interfering with hypothalamic leptin and glucocorticoid signaling",
number = "3",
volume = "68",
doi = "10.2298/ABS151214001N",
pages = "473-481"
}

Radovanović, M., Veličković, N., Đorđević, A., Bursać, B., Macut, Đ., Božić Antić, I., Bjekić Macut, J., Matić, G.,& Vojnović-Milutinović, D.. (2016). 5α-dihydrotestosterone treatment induces metabolic changes associated with Polycystic ovary syndrome without interfering with hypothalamic leptin and glucocorticoid signaling. in Archives of Biological Sciences
Belgrrade: Serbian Biological Society., 68(3), 473-481.
https://doi.org/10.2298/ABS151214001N

Radovanović M, Veličković N, Đorđević A, Bursać B, Macut Đ, Božić Antić I, Bjekić Macut J, Matić G, Vojnović-Milutinović D. 5α-dihydrotestosterone treatment induces metabolic changes associated with Polycystic ovary syndrome without interfering with hypothalamic leptin and glucocorticoid signaling. in Archives of Biological Sciences. 2016;68(3):473-481.
doi:10.2298/ABS151214001N .

Radovanović, Marina, Veličković, Nataša, Đorđević, Ana, Bursać, Biljana, Macut, Đuro, Božić Antić, Ivana, Bjekić Macut, Jelica, Matić, Gordana, Vojnović-Milutinović, Danijela, "5α-dihydrotestosterone treatment induces metabolic changes associated with Polycystic ovary syndrome without interfering with hypothalamic leptin and glucocorticoid signaling" in Archives of Biological Sciences, 68, no. 3 (2016):473-481,
https://doi.org/10.2298/ABS151214001N . .

TY  - THES
AU  - Radovanović, Marina
PY  - 2016
UR  - http://eteze.bg.ac.rs/application/showtheses?thesesId=3045
UR  - https://fedorabg.bg.ac.rs/fedora/get/o:11286/bdef:Content/download
UR  - http://vbs.rs/scripts/cobiss?command=DISPLAY&base=70036&RID=1025053106
UR  - http://nardus.mpn.gov.rs/123456789/5666
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2370
AB  - Sindrom policističnih jajnika (PCOS) je najčešća endokrinopatija žena u reproduktivnom životnom dobu i predstavlja heterogeno oboljenje, koje u osnovi karakterišu hiperandrogenizam, hronična anovulacija i policistični jajnici, a sa njim su povezane i karakteristike metaboličkog sindroma, kao što su insulinska rezistencija, gojaznost, dislipidemija i hipertenzija.Patofiziologija i etiologija PCOS-a, odnosno uzročno-posledična povezanost njegovih pojedinačnih simptoma, nisu do kraja razjašnjene. Generalno se smatra da reproduktivni, endokrini i metabolički poremećaji u PCOS-u formiraju začarani krug u čijem centru je hiperandrogenemija, koju stimulišu visceralna gojaznost, narušen lipidni metabolizam, inflamacija i insulinska rezistencija.Glukokortikoidni hormoni utiču na pojavu visceralne gojaznosti i, delujući antagonistički sa insulinom, mogu da doprinesu patofiziologiji metaboličkog sindroma. Glukokortikoidni hormoni tkivno-specifičnim efektima podstiču nastanak insulinske rezistencije na nivou organizma. Imaju i generalno antiinflamatorna dejstva, ali u gojaznosti podstiču ekspresiju nekih proinflamatornih činilaca.Leptin je hormon masnog tkiva, čija je najvažnija uloga centralno anoreksigeno dejstvo u hipotalamusu tokom kontrole unosa energije. Pri tome, leptin deluje sinergistički sa insulinom i antagonistički sa glukokortikoidnim hormonima. U gojaznosti dolazi do hiperleptinemije i nemogućnosti leptina da ostvari svoje efekte, to jest razvoja leptinske rezistencije. Glukokortikoidi kroz interakcije sa leptinskim signalnim putem mogu da podstaknu njen nastanak...
AB  - Polycystic ovary syndrome (PCOS) is the most common endocrinopathy of women of reproductive age. It is a heterogenous disorder, with hyperandrogenism, chronic anovulation and polycystic ovaries as basic characterisctics, and features of the metabolic syndrome, such as insulin resistance, obesity, dislipidemia and hypertension as associated metabolic characteristics.Pathophysiology and aetiology of PCOS and interlinks between its symptoms are yet to be clarified. It is generally considered that the reproductive, endocrine and metabolic features of PCOS create a vicious circle in the centre of which lies hyperandrogenemia, stimulated by visceral obesity, disturbed lipid metabolism, inflammation and insulin resistance.By functioning antagonistically with insulin, glucocorticoids influence the genesis of visceral obesity and contribute to the pathophysiology of the metabolic syndrome. Their tissue-specific effects stimulate systemic insulin resistance. In addition, glucocorticoids generally exhibit antiinflamatory actions. In obesity, however, they show an ability to stimulate proinflammatory factors.Leptin is a hormone with anorexigenic effects in the hypothalamus. In the course of energy intake and consumption control it works synergistically with insulin, but antagonizes the actions of glucocorticoids. Increased secretion of leptin - hyperleptinemia and leptin resistance are common consequences of obesity...
PB  - Belgrade: University of Belgrade, Faculty of Biology
T2  - University of Belgrade, Faculty of Biology
T1  - Metaboličke karakteristike sindroma policističnih jajnika u visceralnom masnom tkivu i leptinska rezistencija u hipotalamusu pacova tretiranog 5alfa-dihidrotestosteronom: uloga glukokortikosteroida
T1  - Metabolic characteristics of polycistic ovary syndrom in the visceral adipose tissue and leptin resistance in the hypothalamus of the rat treated with 5alfa-dihydrotestosterone: role of glycocorticoids
SP  - 1
EP  - 139
UR  - https://hdl.handle.net/21.15107/rcub_nardus_5666
ER  - 

@phdthesis{
author = "Radovanović, Marina",
year = "2016",
abstract = "Sindrom policističnih jajnika (PCOS) je najčešća endokrinopatija žena u reproduktivnom životnom dobu i predstavlja heterogeno oboljenje, koje u osnovi karakterišu hiperandrogenizam, hronična anovulacija i policistični jajnici, a sa njim su povezane i karakteristike metaboličkog sindroma, kao što su insulinska rezistencija, gojaznost, dislipidemija i hipertenzija.Patofiziologija i etiologija PCOS-a, odnosno uzročno-posledična povezanost njegovih pojedinačnih simptoma, nisu do kraja razjašnjene. Generalno se smatra da reproduktivni, endokrini i metabolički poremećaji u PCOS-u formiraju začarani krug u čijem centru je hiperandrogenemija, koju stimulišu visceralna gojaznost, narušen lipidni metabolizam, inflamacija i insulinska rezistencija.Glukokortikoidni hormoni utiču na pojavu visceralne gojaznosti i, delujući antagonistički sa insulinom, mogu da doprinesu patofiziologiji metaboličkog sindroma. Glukokortikoidni hormoni tkivno-specifičnim efektima podstiču nastanak insulinske rezistencije na nivou organizma. Imaju i generalno antiinflamatorna dejstva, ali u gojaznosti podstiču ekspresiju nekih proinflamatornih činilaca.Leptin je hormon masnog tkiva, čija je najvažnija uloga centralno anoreksigeno dejstvo u hipotalamusu tokom kontrole unosa energije. Pri tome, leptin deluje sinergistički sa insulinom i antagonistički sa glukokortikoidnim hormonima. U gojaznosti dolazi do hiperleptinemije i nemogućnosti leptina da ostvari svoje efekte, to jest razvoja leptinske rezistencije. Glukokortikoidi kroz interakcije sa leptinskim signalnim putem mogu da podstaknu njen nastanak..., Polycystic ovary syndrome (PCOS) is the most common endocrinopathy of women of reproductive age. It is a heterogenous disorder, with hyperandrogenism, chronic anovulation and polycystic ovaries as basic characterisctics, and features of the metabolic syndrome, such as insulin resistance, obesity, dislipidemia and hypertension as associated metabolic characteristics.Pathophysiology and aetiology of PCOS and interlinks between its symptoms are yet to be clarified. It is generally considered that the reproductive, endocrine and metabolic features of PCOS create a vicious circle in the centre of which lies hyperandrogenemia, stimulated by visceral obesity, disturbed lipid metabolism, inflammation and insulin resistance.By functioning antagonistically with insulin, glucocorticoids influence the genesis of visceral obesity and contribute to the pathophysiology of the metabolic syndrome. Their tissue-specific effects stimulate systemic insulin resistance. In addition, glucocorticoids generally exhibit antiinflamatory actions. In obesity, however, they show an ability to stimulate proinflammatory factors.Leptin is a hormone with anorexigenic effects in the hypothalamus. In the course of energy intake and consumption control it works synergistically with insulin, but antagonizes the actions of glucocorticoids. Increased secretion of leptin - hyperleptinemia and leptin resistance are common consequences of obesity...",
publisher = "Belgrade: University of Belgrade, Faculty of Biology",
journal = "University of Belgrade, Faculty of Biology",
title = "Metaboličke karakteristike sindroma policističnih jajnika u visceralnom masnom tkivu i leptinska rezistencija u hipotalamusu pacova tretiranog 5alfa-dihidrotestosteronom: uloga glukokortikosteroida, Metabolic characteristics of polycistic ovary syndrom in the visceral adipose tissue and leptin resistance in the hypothalamus of the rat treated with 5alfa-dihydrotestosterone: role of glycocorticoids",
pages = "1-139",
url = "https://hdl.handle.net/21.15107/rcub_nardus_5666"
}

Radovanović, M.. (2016). Metaboličke karakteristike sindroma policističnih jajnika u visceralnom masnom tkivu i leptinska rezistencija u hipotalamusu pacova tretiranog 5alfa-dihidrotestosteronom: uloga glukokortikosteroida. in University of Belgrade, Faculty of Biology
Belgrade: University of Belgrade, Faculty of Biology., 1-139.
https://hdl.handle.net/21.15107/rcub_nardus_5666

Radovanović M. Metaboličke karakteristike sindroma policističnih jajnika u visceralnom masnom tkivu i leptinska rezistencija u hipotalamusu pacova tretiranog 5alfa-dihidrotestosteronom: uloga glukokortikosteroida. in University of Belgrade, Faculty of Biology. 2016;:1-139.
https://hdl.handle.net/21.15107/rcub_nardus_5666 .

Radovanović, Marina, "Metaboličke karakteristike sindroma policističnih jajnika u visceralnom masnom tkivu i leptinska rezistencija u hipotalamusu pacova tretiranog 5alfa-dihidrotestosteronom: uloga glukokortikosteroida" in University of Belgrade, Faculty of Biology (2016):1-139,
https://hdl.handle.net/21.15107/rcub_nardus_5666 .

TY  - JOUR
AU  - Tepavcevic, Snezana
AU  - Vojnović-Milutinović, Danijela
AU  - Macut, Djuro
AU  - Stojiljkovic, Mojca
AU  - Radovanović, Marina
AU  - Bozic-Antic, Ivana
AU  - Culafic, Tijana
AU  - Bjekić-Macut, Jelica
AU  - Matić, Gordana
AU  - Koricanac, Goran
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1911
AB  - Polycystic ovary syndrome (PCOS) is associated with an altered plasma
   lipid profile and increased risk for cardiovascular diseases. We
   hypothesized that molecular mechanisms underlying cardiac pathology in
   PCOS involve changes in expression and subcellular localization of
   several key proteins involved in cardiac lipid transport and metabolism,
   such as fatty acid transporter CD36, lipin 1, peroxisome
   proliferator-activated receptor alpha (PPAR alpha), peroxisome
   proliferator-activated receptor gamma coactivator-1 (PGC1), and
   carnitine palmitoyltransferase 1 (CPT1). We used the animal model of
   PCOS obtained by treating female rats with dihydrotestosterone (DHT).
   Protein levels of CD36, lipin 1, PPAR alpha, PGC1, and antioxidative
   enzymes were assessed by Western blot in different cardiac cell
   compartments. Cardiac triglycerides (TG) and lipid peroxidation were
   also measured. The content of CD36 was decreased in both the cardiac
   plasma membranes and intracellular pool. On the other hand, total
   content of cardiac lipin 1 in DHT-treated rats was elevated, in contrast
   to decreased microsomal lipin 1 content. An increase in nuclear content
   of lipin 1 was observed together with elevation of nuclear PPAR alpha
   and PGC1, and an increase in CPT1 expression. However, lipid
   peroxidation was reduced in the heart, without alterations in
   antioxidative enzymes expression and cardiac TG content. The results
   indicate that treatment of female rats with DHT is accompanied by a
   decrease of fatty acid uptake and a reduction of lipid peroxidation in
   the heart. The observed elevation of lipin 1, PPAR alpha, PGC1, and CPT1
   expression suggests that cardiac fatty acid metabolism is shifted toward
   mitochondrial beta oxidation.
T2  - Endocrine
T1  - Cardiac fatty acid uptake and metabolism in the rat model of polycystic
 ovary syndrome
IS  - 1
VL  - 50
DO  - 10.1007/s12020-015-0558-1
SP  - 193
EP  - 201
ER  - 

@article{
author = "Tepavcevic, Snezana and Vojnović-Milutinović, Danijela and Macut, Djuro and Stojiljkovic, Mojca and Radovanović, Marina and Bozic-Antic, Ivana and Culafic, Tijana and Bjekić-Macut, Jelica and Matić, Gordana and Koricanac, Goran",
year = "2015",
abstract = "Polycystic ovary syndrome (PCOS) is associated with an altered plasma
   lipid profile and increased risk for cardiovascular diseases. We
   hypothesized that molecular mechanisms underlying cardiac pathology in
   PCOS involve changes in expression and subcellular localization of
   several key proteins involved in cardiac lipid transport and metabolism,
   such as fatty acid transporter CD36, lipin 1, peroxisome
   proliferator-activated receptor alpha (PPAR alpha), peroxisome
   proliferator-activated receptor gamma coactivator-1 (PGC1), and
   carnitine palmitoyltransferase 1 (CPT1). We used the animal model of
   PCOS obtained by treating female rats with dihydrotestosterone (DHT).
   Protein levels of CD36, lipin 1, PPAR alpha, PGC1, and antioxidative
   enzymes were assessed by Western blot in different cardiac cell
   compartments. Cardiac triglycerides (TG) and lipid peroxidation were
   also measured. The content of CD36 was decreased in both the cardiac
   plasma membranes and intracellular pool. On the other hand, total
   content of cardiac lipin 1 in DHT-treated rats was elevated, in contrast
   to decreased microsomal lipin 1 content. An increase in nuclear content
   of lipin 1 was observed together with elevation of nuclear PPAR alpha
   and PGC1, and an increase in CPT1 expression. However, lipid
   peroxidation was reduced in the heart, without alterations in
   antioxidative enzymes expression and cardiac TG content. The results
   indicate that treatment of female rats with DHT is accompanied by a
   decrease of fatty acid uptake and a reduction of lipid peroxidation in
   the heart. The observed elevation of lipin 1, PPAR alpha, PGC1, and CPT1
   expression suggests that cardiac fatty acid metabolism is shifted toward
   mitochondrial beta oxidation.",
journal = "Endocrine",
title = "Cardiac fatty acid uptake and metabolism in the rat model of polycystic
 ovary syndrome",
number = "1",
volume = "50",
doi = "10.1007/s12020-015-0558-1",
pages = "193-201"
}

Tepavcevic, S., Vojnović-Milutinović, D., Macut, D., Stojiljkovic, M., Radovanović, M., Bozic-Antic, I., Culafic, T., Bjekić-Macut, J., Matić, G.,& Koricanac, G.. (2015). Cardiac fatty acid uptake and metabolism in the rat model of polycystic
 ovary syndrome. in Endocrine, 50(1), 193-201.
https://doi.org/10.1007/s12020-015-0558-1

Tepavcevic S, Vojnović-Milutinović D, Macut D, Stojiljkovic M, Radovanović M, Bozic-Antic I, Culafic T, Bjekić-Macut J, Matić G, Koricanac G. Cardiac fatty acid uptake and metabolism in the rat model of polycystic
 ovary syndrome. in Endocrine. 2015;50(1):193-201.
doi:10.1007/s12020-015-0558-1 .

Tepavcevic, Snezana, Vojnović-Milutinović, Danijela, Macut, Djuro, Stojiljkovic, Mojca, Radovanović, Marina, Bozic-Antic, Ivana, Culafic, Tijana, Bjekić-Macut, Jelica, Matić, Gordana, Koricanac, Goran, "Cardiac fatty acid uptake and metabolism in the rat model of polycystic
 ovary syndrome" in Endocrine, 50, no. 1 (2015):193-201,
https://doi.org/10.1007/s12020-015-0558-1 . .

TY  - JOUR
AU  - Radovanović, Marina
AU  - Macut, Đuro
AU  - Đorđević, Ana
AU  - Veličković, Nataša
AU  - Nestorović, Nataša
AU  - Bursać, Biljana
AU  - Božić-Antić, Ivana
AU  - Bjekić Macut, Jelica
AU  - Matić, Gordana
AU  - Vojnović-Milutinović, Danijela
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2022
UR  - https://www.sciencedirect.com/science/article/pii/S0303720714002706?via%3Dihub#ac0010
AB  - Polycystic ovary syndrome (PCOS) is a reproductive and metabolic
   disorder characterized by hyperandrogenism, ovulatory dysfunction,
   visceral obesity and insulin resistance. We hypothesized that changes in
   glucocorticoid metabolism and signaling in the visceral adipose tissue
   may contribute to disturbances of lipid metabolism in the rat model of
   PCOS obtained by 5 alpha-dihydrotestosterone (DHT) treatment of
   prepubertal female Wistar rats. The results confirmed that DHT treatment
   caused anovulation, obesity and dyslipidemia. Enhanced glucocorticoid
   prereceptor metabolism, assessed by elevated intracellular
   corticosterone and increased 11 beta-hydroxysteroid dehydrogenase type 1
   mRNA and protein levels, was accompanied by glucocorticoid receptor (GR)
   nuclear accumulation. In concert with the increased expression of
   GR-regulated prolipogenic genes (lipin-1, sterol regulatory element
   binding protein 1, fatty acid synthase, phosphoenolpyruvate
   carboxykinase), histological analyses revealed hypertrophic adipocytes.
   The results suggest that glucocorticoids influence lipid metabolism in
   the visceral adipose tissue in the way that may contribute to
   pathogenesis of metabolic disturbances associated with PCOS. (C) 2014
   Elsevier Ireland Ltd. All rights reserved.
T2  - Molecular and Cellular Endocrinology
T1  - Possible involvement of glucocorticoids in 5
 alpha-dihydrotestosterone-induced PCOS-like metabolic disturbances in
 the rat visceral adipose tissue
IS  - C
VL  - 399
DO  - 10.1016/j.mce.2014.08.013
SP  - 22
EP  - 31
ER  - 

@article{
author = "Radovanović, Marina and Macut, Đuro and Đorđević, Ana and Veličković, Nataša and Nestorović, Nataša and Bursać, Biljana and Božić-Antić, Ivana and Bjekić Macut, Jelica and Matić, Gordana and Vojnović-Milutinović, Danijela",
year = "2015",
abstract = "Polycystic ovary syndrome (PCOS) is a reproductive and metabolic
   disorder characterized by hyperandrogenism, ovulatory dysfunction,
   visceral obesity and insulin resistance. We hypothesized that changes in
   glucocorticoid metabolism and signaling in the visceral adipose tissue
   may contribute to disturbances of lipid metabolism in the rat model of
   PCOS obtained by 5 alpha-dihydrotestosterone (DHT) treatment of
   prepubertal female Wistar rats. The results confirmed that DHT treatment
   caused anovulation, obesity and dyslipidemia. Enhanced glucocorticoid
   prereceptor metabolism, assessed by elevated intracellular
   corticosterone and increased 11 beta-hydroxysteroid dehydrogenase type 1
   mRNA and protein levels, was accompanied by glucocorticoid receptor (GR)
   nuclear accumulation. In concert with the increased expression of
   GR-regulated prolipogenic genes (lipin-1, sterol regulatory element
   binding protein 1, fatty acid synthase, phosphoenolpyruvate
   carboxykinase), histological analyses revealed hypertrophic adipocytes.
   The results suggest that glucocorticoids influence lipid metabolism in
   the visceral adipose tissue in the way that may contribute to
   pathogenesis of metabolic disturbances associated with PCOS. (C) 2014
   Elsevier Ireland Ltd. All rights reserved.",
journal = "Molecular and Cellular Endocrinology",
title = "Possible involvement of glucocorticoids in 5
 alpha-dihydrotestosterone-induced PCOS-like metabolic disturbances in
 the rat visceral adipose tissue",
number = "C",
volume = "399",
doi = "10.1016/j.mce.2014.08.013",
pages = "22-31"
}

Radovanović, M., Macut, Đ., Đorđević, A., Veličković, N., Nestorović, N., Bursać, B., Božić-Antić, I., Bjekić Macut, J., Matić, G.,& Vojnović-Milutinović, D.. (2015). Possible involvement of glucocorticoids in 5
 alpha-dihydrotestosterone-induced PCOS-like metabolic disturbances in
 the rat visceral adipose tissue. in Molecular and Cellular Endocrinology, 399(C), 22-31.
https://doi.org/10.1016/j.mce.2014.08.013

Radovanović M, Macut Đ, Đorđević A, Veličković N, Nestorović N, Bursać B, Božić-Antić I, Bjekić Macut J, Matić G, Vojnović-Milutinović D. Possible involvement of glucocorticoids in 5
 alpha-dihydrotestosterone-induced PCOS-like metabolic disturbances in
 the rat visceral adipose tissue. in Molecular and Cellular Endocrinology. 2015;399(C):22-31.
doi:10.1016/j.mce.2014.08.013 .

Radovanović, Marina, Macut, Đuro, Đorđević, Ana, Veličković, Nataša, Nestorović, Nataša, Bursać, Biljana, Božić-Antić, Ivana, Bjekić Macut, Jelica, Matić, Gordana, Vojnović-Milutinović, Danijela, "Possible involvement of glucocorticoids in 5
 alpha-dihydrotestosterone-induced PCOS-like metabolic disturbances in
 the rat visceral adipose tissue" in Molecular and Cellular Endocrinology, 399, no. C (2015):22-31,
https://doi.org/10.1016/j.mce.2014.08.013 . .

TY  - JOUR
AU  - Teofilović, Ana
AU  - Bursac, Biljana
AU  - Đorđević, Ana
AU  - Vojnović-Milutinović, Danijela
AU  - Radovanović, Marina
AU  - Matić, Gordana
AU  - Velickovic, Natasa
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2166
AB  - High fructose consumption provokes metabolic perturbations that result
   in chronic low-grade inflammation and insulin resistance.
   Glucocorticoids, potent anti-inflammatory hormones, have important role
   in pathogenesis of diet-induced metabolic disturbances. The aim of this
   study was to examine the link between glucocorticoid metabolism and
   inflammation in the liver of fructose-fed rats.
   Fructose-fed male Wistar rats consumed 60 \% fructose solution for 9
   weeks. Glucocorticoid prereceptor metabolism and signaling were analyzed
   by measuring the level of 11 beta-hydroxysteroid dehydrogenase type 1
   (11 beta HSD1) and hexose-6-phosphate dehydrogenase expression, as well
   as via determination of intracellular corticosterone concentration,
   glucocorticoid receptor subcellular distribution and expression of its
   target gene, phosphoenolpyruvate carboxykinase. Nuclear factor kappa B
   (NF kappa B), tumor necrosis factor alpha (TNF alpha) and the level of
   inhibitory phosphorylation of insulin receptor substrate-1 (IRS-1) on
   Ser(307) were analyzed as markers of hepatic inflammation. The protein
   and/or mRNA levels of all examined molecules were assessed by Western
   blot and/or qPCR.
   Fructose-rich diet led to an enhancement of 11 beta HSD1 protein level
   in the liver, without affecting intracellular level of corticosterone
   and downstream glucocorticoid signaling. On the other hand,
   proinflammatory state was achieved through NF kappa B activation and
   increased TNF alpha expression, while elevated level of inhibitory
   phosphorylation of IRS-1 was observed as an early hallmark of insulin
   resistance.
   High-fructose diet does not influence hepatic glucocorticoid signaling
   downstream of the receptor, permitting development of NF kappa B-driven
   inflammation. The alteration in 11 beta HSD1 expression is most likely
   the consequence of enhanced inflammation, finally leading to disruption
   of insulin signaling in the rat liver.
T2  - European Journal of Nutrition
T1  - Hepatic inflammation induced by high-fructose diet is associated with
 altered 11 beta HSD1 expression in the liver of Wistar rats
IS  - 6
VL  - 53
DO  - 10.1007/s00394-013-0641-4
SP  - 1393
EP  - 1402
ER  - 

@article{
author = "Teofilović, Ana and Bursac, Biljana and Đorđević, Ana and Vojnović-Milutinović, Danijela and Radovanović, Marina and Matić, Gordana and Velickovic, Natasa",
year = "2014",
abstract = "High fructose consumption provokes metabolic perturbations that result
   in chronic low-grade inflammation and insulin resistance.
   Glucocorticoids, potent anti-inflammatory hormones, have important role
   in pathogenesis of diet-induced metabolic disturbances. The aim of this
   study was to examine the link between glucocorticoid metabolism and
   inflammation in the liver of fructose-fed rats.
   Fructose-fed male Wistar rats consumed 60 \% fructose solution for 9
   weeks. Glucocorticoid prereceptor metabolism and signaling were analyzed
   by measuring the level of 11 beta-hydroxysteroid dehydrogenase type 1
   (11 beta HSD1) and hexose-6-phosphate dehydrogenase expression, as well
   as via determination of intracellular corticosterone concentration,
   glucocorticoid receptor subcellular distribution and expression of its
   target gene, phosphoenolpyruvate carboxykinase. Nuclear factor kappa B
   (NF kappa B), tumor necrosis factor alpha (TNF alpha) and the level of
   inhibitory phosphorylation of insulin receptor substrate-1 (IRS-1) on
   Ser(307) were analyzed as markers of hepatic inflammation. The protein
   and/or mRNA levels of all examined molecules were assessed by Western
   blot and/or qPCR.
   Fructose-rich diet led to an enhancement of 11 beta HSD1 protein level
   in the liver, without affecting intracellular level of corticosterone
   and downstream glucocorticoid signaling. On the other hand,
   proinflammatory state was achieved through NF kappa B activation and
   increased TNF alpha expression, while elevated level of inhibitory
   phosphorylation of IRS-1 was observed as an early hallmark of insulin
   resistance.
   High-fructose diet does not influence hepatic glucocorticoid signaling
   downstream of the receptor, permitting development of NF kappa B-driven
   inflammation. The alteration in 11 beta HSD1 expression is most likely
   the consequence of enhanced inflammation, finally leading to disruption
   of insulin signaling in the rat liver.",
journal = "European Journal of Nutrition",
title = "Hepatic inflammation induced by high-fructose diet is associated with
 altered 11 beta HSD1 expression in the liver of Wistar rats",
number = "6",
volume = "53",
doi = "10.1007/s00394-013-0641-4",
pages = "1393-1402"
}

Teofilović, A., Bursac, B., Đorđević, A., Vojnović-Milutinović, D., Radovanović, M., Matić, G.,& Velickovic, N.. (2014). Hepatic inflammation induced by high-fructose diet is associated with
 altered 11 beta HSD1 expression in the liver of Wistar rats. in European Journal of Nutrition, 53(6), 1393-1402.
https://doi.org/10.1007/s00394-013-0641-4

Teofilović A, Bursac B, Đorđević A, Vojnović-Milutinović D, Radovanović M, Matić G, Velickovic N. Hepatic inflammation induced by high-fructose diet is associated with
 altered 11 beta HSD1 expression in the liver of Wistar rats. in European Journal of Nutrition. 2014;53(6):1393-1402.
doi:10.1007/s00394-013-0641-4 .

Teofilović, Ana, Bursac, Biljana, Đorđević, Ana, Vojnović-Milutinović, Danijela, Radovanović, Marina, Matić, Gordana, Velickovic, Natasa, "Hepatic inflammation induced by high-fructose diet is associated with
 altered 11 beta HSD1 expression in the liver of Wistar rats" in European Journal of Nutrition, 53, no. 6 (2014):1393-1402,
https://doi.org/10.1007/s00394-013-0641-4 . .

TY  - JOUR
AU  - Vojnović-Milutinović, Danijela
AU  - Radovanović, Marina
AU  - Dinic, Jovana
AU  - Đorđević, Ana
AU  - Velickovic, Natasa
AU  - Elaković, Ivana
AU  - Matić, Gordana
AU  - Brkljačić, Jelena
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2273
AB  - Alterations in leptin and glucocorticoid signaling pathways in the
   hypothalamus of male and female rats subjected to a fructose-enriched
   diet were studied. The level of expression of the key components of the
   leptin signaling pathway (neuropeptide Y /NPY/ and suppressor of
   cytokine signaling 3 /SOCS3/), and the glucocorticoid signaling pathway
   (glucocorticoid receptor /GR/, 11 beta-hydroxysteroid dehydrogenase type
   1 /11 beta HSD1/ and hexose-6-phosphate dehydrogenase /H6PDH/) did not
   differ between fructose-fed rats and control animals of both genders.
   However, in females, a fructose-enriched diet provoked increases in the
   adiposity index, plasma leptin and triglyceride concentrations, and
   displayed a tendency to decrease the leptin receptor (ObRb) protein and
   mRNA levels. In male rats, the fructose diet caused elevations in plasma
   non-esterified fatty acids and triglycerides, as well as in both plasma
   and hypothalamic leptin concentrations. Our results suggest that a
   fructose-enriched diet can induce hyperleptinemia in both female and
   male rats, but with a more pronounced effect on hypothalamic leptin
   sensitivity in females, probably contributing to the observed
   development of visceral adiposity.
T2  - Archives of Biological Sciences
T1  - Leptin and glucocorticoid signaling pathways in the hypothalamus of female and male fructose-fed rats
IS  - 2
VL  - 66
DO  - 10.2298/ABS1402829M
SP  - 829
EP  - 839
ER  - 

@article{
author = "Vojnović-Milutinović, Danijela and Radovanović, Marina and Dinic, Jovana and Đorđević, Ana and Velickovic, Natasa and Elaković, Ivana and Matić, Gordana and Brkljačić, Jelena",
year = "2014",
abstract = "Alterations in leptin and glucocorticoid signaling pathways in the
   hypothalamus of male and female rats subjected to a fructose-enriched
   diet were studied. The level of expression of the key components of the
   leptin signaling pathway (neuropeptide Y /NPY/ and suppressor of
   cytokine signaling 3 /SOCS3/), and the glucocorticoid signaling pathway
   (glucocorticoid receptor /GR/, 11 beta-hydroxysteroid dehydrogenase type
   1 /11 beta HSD1/ and hexose-6-phosphate dehydrogenase /H6PDH/) did not
   differ between fructose-fed rats and control animals of both genders.
   However, in females, a fructose-enriched diet provoked increases in the
   adiposity index, plasma leptin and triglyceride concentrations, and
   displayed a tendency to decrease the leptin receptor (ObRb) protein and
   mRNA levels. In male rats, the fructose diet caused elevations in plasma
   non-esterified fatty acids and triglycerides, as well as in both plasma
   and hypothalamic leptin concentrations. Our results suggest that a
   fructose-enriched diet can induce hyperleptinemia in both female and
   male rats, but with a more pronounced effect on hypothalamic leptin
   sensitivity in females, probably contributing to the observed
   development of visceral adiposity.",
journal = "Archives of Biological Sciences",
title = "Leptin and glucocorticoid signaling pathways in the hypothalamus of female and male fructose-fed rats",
number = "2",
volume = "66",
doi = "10.2298/ABS1402829M",
pages = "829-839"
}

Vojnović-Milutinović, D., Radovanović, M., Dinic, J., Đorđević, A., Velickovic, N., Elaković, I., Matić, G.,& Brkljačić, J.. (2014). Leptin and glucocorticoid signaling pathways in the hypothalamus of female and male fructose-fed rats. in Archives of Biological Sciences, 66(2), 829-839.
https://doi.org/10.2298/ABS1402829M

Vojnović-Milutinović D, Radovanović M, Dinic J, Đorđević A, Velickovic N, Elaković I, Matić G, Brkljačić J. Leptin and glucocorticoid signaling pathways in the hypothalamus of female and male fructose-fed rats. in Archives of Biological Sciences. 2014;66(2):829-839.
doi:10.2298/ABS1402829M .

Vojnović-Milutinović, Danijela, Radovanović, Marina, Dinic, Jovana, Đorđević, Ana, Velickovic, Natasa, Elaković, Ivana, Matić, Gordana, Brkljačić, Jelena, "Leptin and glucocorticoid signaling pathways in the hypothalamus of female and male fructose-fed rats" in Archives of Biological Sciences, 66, no. 2 (2014):829-839,
https://doi.org/10.2298/ABS1402829M . .

TY  - JOUR
AU  - Tepavcevic, Snezana
AU  - Vojnović-Milutinović, Danijela
AU  - Macut, Djuro
AU  - Zakula, Zorica
AU  - Radovanović, Marina
AU  - Bozic-Antic, Ivana
AU  - Romic, Snjezana
AU  - Bjekić-Macut, Jelica
AU  - Matić, Gordana
AU  - Koricanac, Goran
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2217
AB  - It is supposed that women with polycystic ovary syndrome (PCOS) are
   prone to develop cardiovascular disease as a consequence of multiple
   risk factors that are mostly related to the state of insulin resistance
   and consequent hyperinsulinemia. In the present study, we evaluated
   insulin signaling and glucose transporters (GLUT) in cardiac cells of
   dihydrotestosterone (DHT) treated female rats as an animal model of
   PCOS. Expression of proteins involved in cardiac insulin signaling
   pathways and glucose transporters, as well as their phosphorylation or
   intracellular localization were studied by Western blot analysis in
   DHT-treated and control rats. Treatment with DHT resulted in increased
   body mass, absolute mass of the heart, elevated plasma insulin
   concentration, dyslipidemia and insulin resistance. At the molecular
   level, DHT treatment did not change protein expression of cardiac
   insulin receptor and insulin receptor substrate 1, while phosphorylation
   of the substrate at serine 307 was increased. Unexpectedly, although
   expression of downstream Akt kinase and its phosphorylation at threonine
   308 were not altered, phosphoiylation of Akt at serine 473 was increased
   in the heart of DHT-treated rats. In contrast, expression and
   phosphorylation of extracellular signal regulated kinases 1/2 were
   decreased. Plasma membrane contents of GLUT1 and GLUT4 were decreased,
   as well as the expression of GLUT4 in cardiac cells at the end of
   androgen treatment. The obtained results provide evidence for
   alterations in expression and especially in functional characteristics
   of insulin signaling molecules and glucose transporters in the heart of
   DHT-treated rats with PCOS, indicating impaired cardiac insulin action.
   (c) 2014 Elsevier Ltd. All rights reserved.
T2  - Journal of Steroid Biochemistry and Molecular Biology
T1  - Dihydrotestosterone deteriorates cardiac insulin signaling and glucose
 transport in the rat model of polycystic ovary syndrome
VL  - 141
DO  - 10.1016/j.jsbmb.2014.01.006
SP  - 71
EP  - 76
ER  - 

@article{
author = "Tepavcevic, Snezana and Vojnović-Milutinović, Danijela and Macut, Djuro and Zakula, Zorica and Radovanović, Marina and Bozic-Antic, Ivana and Romic, Snjezana and Bjekić-Macut, Jelica and Matić, Gordana and Koricanac, Goran",
year = "2014",
abstract = "It is supposed that women with polycystic ovary syndrome (PCOS) are
   prone to develop cardiovascular disease as a consequence of multiple
   risk factors that are mostly related to the state of insulin resistance
   and consequent hyperinsulinemia. In the present study, we evaluated
   insulin signaling and glucose transporters (GLUT) in cardiac cells of
   dihydrotestosterone (DHT) treated female rats as an animal model of
   PCOS. Expression of proteins involved in cardiac insulin signaling
   pathways and glucose transporters, as well as their phosphorylation or
   intracellular localization were studied by Western blot analysis in
   DHT-treated and control rats. Treatment with DHT resulted in increased
   body mass, absolute mass of the heart, elevated plasma insulin
   concentration, dyslipidemia and insulin resistance. At the molecular
   level, DHT treatment did not change protein expression of cardiac
   insulin receptor and insulin receptor substrate 1, while phosphorylation
   of the substrate at serine 307 was increased. Unexpectedly, although
   expression of downstream Akt kinase and its phosphorylation at threonine
   308 were not altered, phosphoiylation of Akt at serine 473 was increased
   in the heart of DHT-treated rats. In contrast, expression and
   phosphorylation of extracellular signal regulated kinases 1/2 were
   decreased. Plasma membrane contents of GLUT1 and GLUT4 were decreased,
   as well as the expression of GLUT4 in cardiac cells at the end of
   androgen treatment. The obtained results provide evidence for
   alterations in expression and especially in functional characteristics
   of insulin signaling molecules and glucose transporters in the heart of
   DHT-treated rats with PCOS, indicating impaired cardiac insulin action.
   (c) 2014 Elsevier Ltd. All rights reserved.",
journal = "Journal of Steroid Biochemistry and Molecular Biology",
title = "Dihydrotestosterone deteriorates cardiac insulin signaling and glucose
 transport in the rat model of polycystic ovary syndrome",
volume = "141",
doi = "10.1016/j.jsbmb.2014.01.006",
pages = "71-76"
}

Tepavcevic, S., Vojnović-Milutinović, D., Macut, D., Zakula, Z., Radovanović, M., Bozic-Antic, I., Romic, S., Bjekić-Macut, J., Matić, G.,& Koricanac, G.. (2014). Dihydrotestosterone deteriorates cardiac insulin signaling and glucose
 transport in the rat model of polycystic ovary syndrome. in Journal of Steroid Biochemistry and Molecular Biology, 141, 71-76.
https://doi.org/10.1016/j.jsbmb.2014.01.006

Tepavcevic S, Vojnović-Milutinović D, Macut D, Zakula Z, Radovanović M, Bozic-Antic I, Romic S, Bjekić-Macut J, Matić G, Koricanac G. Dihydrotestosterone deteriorates cardiac insulin signaling and glucose
 transport in the rat model of polycystic ovary syndrome. in Journal of Steroid Biochemistry and Molecular Biology. 2014;141:71-76.
doi:10.1016/j.jsbmb.2014.01.006 .

Tepavcevic, Snezana, Vojnović-Milutinović, Danijela, Macut, Djuro, Zakula, Zorica, Radovanović, Marina, Bozic-Antic, Ivana, Romic, Snjezana, Bjekić-Macut, Jelica, Matić, Gordana, Koricanac, Goran, "Dihydrotestosterone deteriorates cardiac insulin signaling and glucose
 transport in the rat model of polycystic ovary syndrome" in Journal of Steroid Biochemistry and Molecular Biology, 141 (2014):71-76,
https://doi.org/10.1016/j.jsbmb.2014.01.006 . .

TY  - JOUR
AU  - Vojnović-Milutinović, Danijela
AU  - Macut, Djuro
AU  - Bozic-Antic, Ivana
AU  - Macut, Jelica Bjekic
AU  - Radovanović, Marina
AU  - Matić, Gordana
AU  - Brkljačić, Jelena
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2157
AB  - Background: The polycystic ovary syndrome (PCOS) is a frequent endocrine
   disorder that affects women of reproductive age. As the syndrome is
   strongly associated with obesity, it is of interest to examine the gene
   expression differences that accompany its development and the associated
   metabolic disturbances. Real-time RT PCR is a standard method for
   studying changes in gene expression. However, to obtain accurate and
   reliable results, validation of reference genes is obligatory. The aim
   of this study was to identify a suitable reference for the normalization
   of gene expression in peripheral blood mononuclear cells (PBMCs) from
   obese and normal-weight women with PCOS.
   Methods: The expression stability of four potential reference genes:
   hypoxanthine guanine phosphoribosyl transferase 1 (HPRT), beta-actin
   (BA), beta(2)-microglobulin (B2M) and glyceraldehyde-3-phosphate
   dehydrogenase (GAPDH), was assessed in PBMCs from healthy women, and
   from normal-weight and obese women with PCOS. The variability in the
   expression of potential reference genes was analyzed by the TaqMan
   real-time RT PCR method, using GeNorm and Norm Finder software packages.
   Results: Direct comparison of cycle threshold (Ct) values showed
   inter-individual variations for all validated genes, the Ct values of
   HPRT being less variable than those of BA, GAPDH and B2M. Both software
   packages pointed to HPRT as the most steadily expressed gene in the
   PBMCs of women with PCOS and healthy controls.
   Conclusions: Cross-validation of the expression stability of four
   potential reference genes identified HPRT as the most stable reference,
   suitable for further investigations of gene expression in PBMCs from
   women with PCOS.
T2  - Journal of Medical Biochemistry
T1  - Hypoxanthine Guanine Phosphoribosyl Transferase Is the Most Stable Reference Gene for Gene Expression Analysis by Quantitative PCR in Peripheral Blood Mononuclear Cells from Women with the Polycystic Ovary Syndrome
IS  - 4
VL  - 33
DO  - 10.2478/jomb-2014-0029
SP  - 356
EP  - 363
ER  - 

@article{
author = "Vojnović-Milutinović, Danijela and Macut, Djuro and Bozic-Antic, Ivana and Macut, Jelica Bjekic and Radovanović, Marina and Matić, Gordana and Brkljačić, Jelena",
year = "2014",
abstract = "Background: The polycystic ovary syndrome (PCOS) is a frequent endocrine
   disorder that affects women of reproductive age. As the syndrome is
   strongly associated with obesity, it is of interest to examine the gene
   expression differences that accompany its development and the associated
   metabolic disturbances. Real-time RT PCR is a standard method for
   studying changes in gene expression. However, to obtain accurate and
   reliable results, validation of reference genes is obligatory. The aim
   of this study was to identify a suitable reference for the normalization
   of gene expression in peripheral blood mononuclear cells (PBMCs) from
   obese and normal-weight women with PCOS.
   Methods: The expression stability of four potential reference genes:
   hypoxanthine guanine phosphoribosyl transferase 1 (HPRT), beta-actin
   (BA), beta(2)-microglobulin (B2M) and glyceraldehyde-3-phosphate
   dehydrogenase (GAPDH), was assessed in PBMCs from healthy women, and
   from normal-weight and obese women with PCOS. The variability in the
   expression of potential reference genes was analyzed by the TaqMan
   real-time RT PCR method, using GeNorm and Norm Finder software packages.
   Results: Direct comparison of cycle threshold (Ct) values showed
   inter-individual variations for all validated genes, the Ct values of
   HPRT being less variable than those of BA, GAPDH and B2M. Both software
   packages pointed to HPRT as the most steadily expressed gene in the
   PBMCs of women with PCOS and healthy controls.
   Conclusions: Cross-validation of the expression stability of four
   potential reference genes identified HPRT as the most stable reference,
   suitable for further investigations of gene expression in PBMCs from
   women with PCOS.",
journal = "Journal of Medical Biochemistry",
title = "Hypoxanthine Guanine Phosphoribosyl Transferase Is the Most Stable Reference Gene for Gene Expression Analysis by Quantitative PCR in Peripheral Blood Mononuclear Cells from Women with the Polycystic Ovary Syndrome",
number = "4",
volume = "33",
doi = "10.2478/jomb-2014-0029",
pages = "356-363"
}

Vojnović-Milutinović, D., Macut, D., Bozic-Antic, I., Macut, J. B., Radovanović, M., Matić, G.,& Brkljačić, J.. (2014). Hypoxanthine Guanine Phosphoribosyl Transferase Is the Most Stable Reference Gene for Gene Expression Analysis by Quantitative PCR in Peripheral Blood Mononuclear Cells from Women with the Polycystic Ovary Syndrome. in Journal of Medical Biochemistry, 33(4), 356-363.
https://doi.org/10.2478/jomb-2014-0029

Vojnović-Milutinović D, Macut D, Bozic-Antic I, Macut JB, Radovanović M, Matić G, Brkljačić J. Hypoxanthine Guanine Phosphoribosyl Transferase Is the Most Stable Reference Gene for Gene Expression Analysis by Quantitative PCR in Peripheral Blood Mononuclear Cells from Women with the Polycystic Ovary Syndrome. in Journal of Medical Biochemistry. 2014;33(4):356-363.
doi:10.2478/jomb-2014-0029 .

Vojnović-Milutinović, Danijela, Macut, Djuro, Bozic-Antic, Ivana, Macut, Jelica Bjekic, Radovanović, Marina, Matić, Gordana, Brkljačić, Jelena, "Hypoxanthine Guanine Phosphoribosyl Transferase Is the Most Stable Reference Gene for Gene Expression Analysis by Quantitative PCR in Peripheral Blood Mononuclear Cells from Women with the Polycystic Ovary Syndrome" in Journal of Medical Biochemistry, 33, no. 4 (2014):356-363,
https://doi.org/10.2478/jomb-2014-0029 . .