TY  - JOUR
AU  - Šumarac-Dumanović, Mirjana
AU  - Apostolović, Milica
AU  - Janjetović, Kristina
AU  - Jeremić, Danka
AU  - Popadić, Dušan
AU  - Ljubić, Aleksandar
AU  - Micić, Jelena
AU  - Dukanac-Stamenković, Jelena
AU  - Tubić, Aleksandra
AU  - Stevanović, Darko
AU  - Micić, Dragan
AU  - Trajković, Vladimir
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6352
AB  - Autophagy, a process of controlled cellular self-digestion, could be involved in cyclic remodeling
of the human endometrium. We investigated endometrial mRNA expression of 23 autophagyrelated
(ATG) genes and transcription factors in healthy controls (n = 12) and anovulatory
polycystic ovary syndrome (PCOS) patients (n = 24), as well as in their subgroup (n = 12) before
and after metformin treatment. The mRNA levels of transcription factor forkhead box protein O1
(FOXO1) and several molecules involved in autophagosome formation (ATG13, RB1-inducible
coiled-coil 1), autophagosome nucleation (ATG14, beclin 1, SH3-domain GRB2-like endophilin
B1), autophagosome elongation (ATG3, ATG5, g-aminobutyric acid receptor-associated protein -
GABARAP), and delivery of ubiquitinated proteins to autophagosomes (sequestosome 1), were
significantly reduced in anovulatory PCOS compared to healthy endometrium. Free androgen
index, but not free estrogen index, insulin levels, or BMI, negatively correlated with the
endometrial expression of ATG3, ATG14, and GABARAP in PCOS patients. Treatment of
PCOS patients with metformin (2 g/day for 3 months) significantly increased the endometrial
mRNA levels of FOXO1, ATG3, and UV radiation resistance-associated gene. These data
suggest that increased androgen availability in PCOS is associated with metformin-sensitive
transcriptional downregulation of endometrial autophagy
PB  - Elsevier
T2  - Molecular and Cellular Endocrinology
T1  - Downregulation of autophagy gene expression in endometria from women with polycystic ovary syndrome
VL  - 440
DO  - 10.1016/j.mce.2016.11.009
SP  - 116
EP  - 124
ER  - 

@article{
author = "Šumarac-Dumanović, Mirjana and Apostolović, Milica and Janjetović, Kristina and Jeremić, Danka and Popadić, Dušan and Ljubić, Aleksandar and Micić, Jelena and Dukanac-Stamenković, Jelena and Tubić, Aleksandra and Stevanović, Darko and Micić, Dragan and Trajković, Vladimir",
year = "2017",
abstract = "Autophagy, a process of controlled cellular self-digestion, could be involved in cyclic remodeling
of the human endometrium. We investigated endometrial mRNA expression of 23 autophagyrelated
(ATG) genes and transcription factors in healthy controls (n = 12) and anovulatory
polycystic ovary syndrome (PCOS) patients (n = 24), as well as in their subgroup (n = 12) before
and after metformin treatment. The mRNA levels of transcription factor forkhead box protein O1
(FOXO1) and several molecules involved in autophagosome formation (ATG13, RB1-inducible
coiled-coil 1), autophagosome nucleation (ATG14, beclin 1, SH3-domain GRB2-like endophilin
B1), autophagosome elongation (ATG3, ATG5, g-aminobutyric acid receptor-associated protein -
GABARAP), and delivery of ubiquitinated proteins to autophagosomes (sequestosome 1), were
significantly reduced in anovulatory PCOS compared to healthy endometrium. Free androgen
index, but not free estrogen index, insulin levels, or BMI, negatively correlated with the
endometrial expression of ATG3, ATG14, and GABARAP in PCOS patients. Treatment of
PCOS patients with metformin (2 g/day for 3 months) significantly increased the endometrial
mRNA levels of FOXO1, ATG3, and UV radiation resistance-associated gene. These data
suggest that increased androgen availability in PCOS is associated with metformin-sensitive
transcriptional downregulation of endometrial autophagy",
publisher = "Elsevier",
journal = "Molecular and Cellular Endocrinology",
title = "Downregulation of autophagy gene expression in endometria from women with polycystic ovary syndrome",
volume = "440",
doi = "10.1016/j.mce.2016.11.009",
pages = "116-124"
}

Šumarac-Dumanović, M., Apostolović, M., Janjetović, K., Jeremić, D., Popadić, D., Ljubić, A., Micić, J., Dukanac-Stamenković, J., Tubić, A., Stevanović, D., Micić, D.,& Trajković, V.. (2017). Downregulation of autophagy gene expression in endometria from women with polycystic ovary syndrome. in Molecular and Cellular Endocrinology
Elsevier., 440, 116-124.
https://doi.org/10.1016/j.mce.2016.11.009

Šumarac-Dumanović M, Apostolović M, Janjetović K, Jeremić D, Popadić D, Ljubić A, Micić J, Dukanac-Stamenković J, Tubić A, Stevanović D, Micić D, Trajković V. Downregulation of autophagy gene expression in endometria from women with polycystic ovary syndrome. in Molecular and Cellular Endocrinology. 2017;440:116-124.
doi:10.1016/j.mce.2016.11.009 .

Šumarac-Dumanović, Mirjana, Apostolović, Milica, Janjetović, Kristina, Jeremić, Danka, Popadić, Dušan, Ljubić, Aleksandar, Micić, Jelena, Dukanac-Stamenković, Jelena, Tubić, Aleksandra, Stevanović, Darko, Micić, Dragan, Trajković, Vladimir, "Downregulation of autophagy gene expression in endometria from women with polycystic ovary syndrome" in Molecular and Cellular Endocrinology, 440 (2017):116-124,
https://doi.org/10.1016/j.mce.2016.11.009 . .

TY  - JOUR
AU  - Stevanović, Darko
AU  - Trajković, Vladimir
AU  - Müller-Lühlhoff, Sabrina
AU  - Brandt, Elisabeth
AU  - Abplanalp, William
AU  - Bumke-Vogt, Christiane
AU  - Liehl, Beate
AU  - Wiedmer, Petra
AU  - Janjetović, Kristina
AU  - Starčević, Vesna
AU  - Pfeiffer, Andreas F.H.
AU  - Al-Hasani, Hadi
AU  - Tschöp, Matthias H.
AU  - Castañeda, Tamara R.
PY  - 2013
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6350
AB  - Signaling through the mammalian target of rapamycin complex 1 (mTORC1) and its effectors the S6-
kinases (S6K) in the hypothalamus is thought to be involved in nutrient sensing and control of food
intake. Given the anatomical proximity of this pathway to circuits for the hormone ghrelin, we investigated
the potential role of the mTORC1/S6K pathway in mediating the metabolic effects of ghrelin. We
found that ghrelin promoted phosphorylation of S6K1 in the mouse hypothalamic cell line N-41 and in
the rat hypothalamus after intracerebroventricular administration. Rapamycin, an inhibitor of mTORC1,
suppressed ghrelin-induced phosphorylation of hypothalamic S6K1 and increased food intake and insulin
in rats. Chronic peripheral administration of ghrelin induced a significant increase in body weight, fat
mass and food efficiency in wild-type and S6K2-knockout but not in S6K1-knockout mice. We therefore
propose that ghrelin-induced hyperphagia, adiposity and insulin secretion are controlled by a central nervous system involving the mTORC1/S6K1 pathway.
PB  - Elsevier
T2  - Molecular and Cellular Endocrinology
T1  - Ghrelin-induced food intake and adiposity depend on central mTORC1/S6K1 signaling
IS  - 1-2
VL  - 381
DO  - 10.1016/j.mce.2013.08.009
SP  - 280
EP  - 290
ER  - 

@article{
author = "Stevanović, Darko and Trajković, Vladimir and Müller-Lühlhoff, Sabrina and Brandt, Elisabeth and Abplanalp, William and Bumke-Vogt, Christiane and Liehl, Beate and Wiedmer, Petra and Janjetović, Kristina and Starčević, Vesna and Pfeiffer, Andreas F.H. and Al-Hasani, Hadi and Tschöp, Matthias H. and Castañeda, Tamara R.",
year = "2013",
abstract = "Signaling through the mammalian target of rapamycin complex 1 (mTORC1) and its effectors the S6-
kinases (S6K) in the hypothalamus is thought to be involved in nutrient sensing and control of food
intake. Given the anatomical proximity of this pathway to circuits for the hormone ghrelin, we investigated
the potential role of the mTORC1/S6K pathway in mediating the metabolic effects of ghrelin. We
found that ghrelin promoted phosphorylation of S6K1 in the mouse hypothalamic cell line N-41 and in
the rat hypothalamus after intracerebroventricular administration. Rapamycin, an inhibitor of mTORC1,
suppressed ghrelin-induced phosphorylation of hypothalamic S6K1 and increased food intake and insulin
in rats. Chronic peripheral administration of ghrelin induced a significant increase in body weight, fat
mass and food efficiency in wild-type and S6K2-knockout but not in S6K1-knockout mice. We therefore
propose that ghrelin-induced hyperphagia, adiposity and insulin secretion are controlled by a central nervous system involving the mTORC1/S6K1 pathway.",
publisher = "Elsevier",
journal = "Molecular and Cellular Endocrinology",
title = "Ghrelin-induced food intake and adiposity depend on central mTORC1/S6K1 signaling",
number = "1-2",
volume = "381",
doi = "10.1016/j.mce.2013.08.009",
pages = "280-290"
}

Stevanović, D., Trajković, V., Müller-Lühlhoff, S., Brandt, E., Abplanalp, W., Bumke-Vogt, C., Liehl, B., Wiedmer, P., Janjetović, K., Starčević, V., Pfeiffer, A. F.H., Al-Hasani, H., Tschöp, M. H.,& Castañeda, T. R.. (2013). Ghrelin-induced food intake and adiposity depend on central mTORC1/S6K1 signaling. in Molecular and Cellular Endocrinology
Elsevier., 381(1-2), 280-290.
https://doi.org/10.1016/j.mce.2013.08.009

Stevanović D, Trajković V, Müller-Lühlhoff S, Brandt E, Abplanalp W, Bumke-Vogt C, Liehl B, Wiedmer P, Janjetović K, Starčević V, Pfeiffer AF, Al-Hasani H, Tschöp MH, Castañeda TR. Ghrelin-induced food intake and adiposity depend on central mTORC1/S6K1 signaling. in Molecular and Cellular Endocrinology. 2013;381(1-2):280-290.
doi:10.1016/j.mce.2013.08.009 .

Stevanović, Darko, Trajković, Vladimir, Müller-Lühlhoff, Sabrina, Brandt, Elisabeth, Abplanalp, William, Bumke-Vogt, Christiane, Liehl, Beate, Wiedmer, Petra, Janjetović, Kristina, Starčević, Vesna, Pfeiffer, Andreas F.H., Al-Hasani, Hadi, Tschöp, Matthias H., Castañeda, Tamara R., "Ghrelin-induced food intake and adiposity depend on central mTORC1/S6K1 signaling" in Molecular and Cellular Endocrinology, 381, no. 1-2 (2013):280-290,
https://doi.org/10.1016/j.mce.2013.08.009 . .