scholarly journals Insulin and Messenger Ribonucleic Acid Expression of Insulin Receptor Isoforms in Ovarian Follicles from Nonhirsute Ovulatory Women and Polycystic Ovary Syndrome Patients

2004 ◽  
Vol 89 (7) ◽  
pp. 3561-3566 ◽  
Author(s):  
Jennifer L. Phy ◽  
Cheryl A. Conover ◽  
David H. Abbott ◽  
Michael A. Zschunke ◽  
David L. Walker ◽  
...  
2018 ◽  
Vol 30 (4) ◽  
pp. 571 ◽  
Author(s):  
Anusha Singh ◽  
Puran Bora ◽  
Amitabh Krishna

The present study examined the efficacy of adiponectin for regulating the reproductive, metabolic and fertility status of mice with polycystic ovary syndrome (PCOS). PCOS was induced in prepubertal (21- to 22-day-old) mice using dehydroepiandrosterone (6 mg 100 g−1 day−1 for 25 days), after which mice were administered either a low or high dose of adiponectin (5 or 15 µg mL−1, s.c., respectively). PCOS mice exhibited typical features, including the presence of numerous cystic follicles, increased circulating androgens, increased body mass, altered steroidogenesis, decreased insulin receptor expression and increased serum triglycerides, serum glucose, Toll-like receptor (TLR)-4 (a marker of inflammation) and vascular endothelial growth factor (VEGF; a marker of angiogenesis). These parameters were significantly correlated with a reduction in adiponectin in PCOS mice compared with vehicle-treated control mice. Exogenous adiponectin treatment of PCOS mice restored body mass and circulating androgen, triglyceride and glucose levels. Adiponectin also restored ovarian expression of steroidogenic markers (LH receptors, steroidogenic acute regulatory protein and 3β-hydroxysteroid dehydrogenase), insulin receptor, TLR-4 and VEGF levels in control mice. Adiponectin restored ovulation in PCOS mice, as indicated by the presence of a corpus luteum and attainment of pregnancy. These findings suggest that adiponectin effectively facilitates fertility in anovulatory PCOS. We hypothesise that systemic adiponectin treatment may be a promising therapeutic strategy for the management of PCOS.


2001 ◽  
Vol 281 (2) ◽  
pp. E392-E399 ◽  
Author(s):  
Andrea Dunaif ◽  
Xinqi Wu ◽  
Anna Lee ◽  
Evanthia Diamanti-Kandarakis

Women with polycystic ovary syndrome (PCOS) are insulin resistant secondary to a postbinding defect in insulin signaling. Sequential euglycemic glucose clamp studies at 40 and 400 mU · m−2 · min−1 insulin doses with serial skeletal muscle biopsies were performed in PCOS and age-, weight-, and ethnicity-matched control women. Steady-state insulin levels did not differ, but insulin-mediated glucose disposal was significantly decreased in PCOS women ( P < 0.05). Insulin receptor substrate (IRS)-1-associated phosphatidylinositol 3-kinase (PI 3K) activity was significantly decreased in PCOS ( n = 12) compared with control skeletal muscle ( n = 8; P < 0.05). There was no significant difference in the abundance of IR, IRS-1, or the p85 regulatory subunit of PI 3K in PCOS ( n = 14) compared with control ( n = 12) muscle. The abundance of IRS-2 was significantly increased ( P < 0.05) in PCOS skeletal muscle, suggesting a compensatory change. We conclude that there is a physiologically relevant defect in insulin receptor signaling in PCOS that is independent of obesity and type 2 diabetes mellitus.


2003 ◽  
Vol 79 (1) ◽  
pp. 219-220 ◽  
Author(s):  
Gemma Villuendas ◽  
H.éctor F Escobar-Morreale ◽  
Flavia Tosi ◽  
José Sancho ◽  
Paolo Moghetti ◽  
...  

2008 ◽  
Vol 390 (1-2) ◽  
pp. 63-66 ◽  
Author(s):  
Patricio Valdés ◽  
Alvaro Cerda ◽  
Cristobal Barrenechea ◽  
Marlene Kehr ◽  
Carolina Soto ◽  
...  

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