Macut, Đuro

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  • Macut, Đuro (1)
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Author's Bibliography

5α-dihydrotestosterone treatment induces metabolic changes associated with Polycystic ovary syndrome without interfering with hypothalamic leptin and glucocorticoid signaling

Radovanović, Marina; Veličković, Nataša; Đorđević, Ana; Bursać, Biljana; Macut, Đuro; Božić Antić, Ivana; Bjekić Macut, Jelica; Matić, Gordana; Vojnović-Milutinović, Danijela

(Belgrrade: Serbian Biological Society, 2016)

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 . .
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