Insulin stimulates testosterone biosynthesis by human thecal cells from women with polycystic ovary syndrome by activating its own receptor and using inositolglycan mediators as the signal transduction system.
TL;DR: It is suggested that inositolglycans serve as the signal transduction system for insulin's stimulation of human thecal testosterone biosynthesis.
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Abstract: To determine whether insulin stimulates human ovarian testosterone production in the polycystic ovary syndrome by activating its own receptor and using inositolglycan mediators as the signal transduction system, thecal cells from polycystic ovary syndrome women were isolated and cultured. Insulin and insulin-like growth factor I stimulated thecal testosterone biosynthesis. Antibody blockade of the insulin receptor abolished insulin's stimulatory action, whereas effective antibody blockade of the insulin-like growth factor I receptor did not alter insulin's stimulation of thecal testosterone biosynthesis. A chiro-inositol containing glycan (INS-2) increased thecal testosterone biosynthesis. Preincubation of cells with an antiinositolglycan antibody (A23939 or alpha IGP) abolished insulin's stimulatory effect, but not that of hCG. These findings suggest that inositolglycans serve as the signal transduction system for insulin's stimulation of human thecal testosterone biosynthesis.
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Differentiating Polycystic Ovary Syndrome from Adrenal Disorders
TL;DR: The pathophysiology of androgen excess of both adrenal and ovarian origins is discussed; the conditions which lead to androgens excess are outlined; and the differential diagnosis of PCOS from certain adrenal disorders is facilitated.
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TL;DR: These studies show that there are significant strain-related differences in metabolic response to excess androgen exposure during puberty and suggest the C57BL/6J strain provides a more robust and uniform experimental platform for PCOS research than the BALB/cByJ strain.
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Metformin therapy in polycystic ovary syndrome reduces hyperinsulinemia, insulin resistance, hyperandrogenemia, and systolic blood pressure, while facilitating normal menses and pregnancy☆
E.M. Velazquez,Soaira Mendoza,Soaira Mendoza,Tracy Hamer,Tracy Hamer,Felix Sosa,Felix Sosa,Charles J. Glueck,Charles J. Glueck +8 more
TL;DR: Using polycystic ovary syndrome as a model of insulin resistance and hyperandrogenism, the effect of Metformin on lipoproteins, sex hormones, gonadotropins, and blood pressure in 26 women with PCOS was assessed.
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Polycystic Ovary Syndrome
Stephen Franks
- 01 Apr 2007
TL;DR: It is of interest to realize that polycystic ovary syndrome has moved from a histology diagnosis of ovarian tissue to a heterogeneous clinical syndrome, to a reproductive endocrine abnormality with elevated serum luteinizing hormone and androgen levels, and to a metabolic disease characterized by hyperinsulinemia and dyslipidemia.
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Phosphatidylinositol-glycan anchors of membrane proteins: potential precursors of insulin mediators.
Guillermo Romero,Louis M. Luttrell,Alan D. Rogol,Konrad Zeller,Erik L. Hewlett,Joseph Larner +5 more
TL;DR: A new model of insulin action is suggested by showing that alkaline phosphatase release and dimyristoylglycerol production are independent processes and that the blockade of either event inhibits the production of insulin mediator.
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17α-Hydroxyprogesterone Responses to Leuprolide and Serum Androgens in Obese Women with and without Polycystic Ovary Syndrome after Dietary Weight Loss1
TL;DR: Serum insulin decreased in both PCOS and control groups and serum steroid concentrations and 17α-hydroxyprogesterone responses to leuprolide administration decreased, suggesting weight loss would decrease serum insulin and P450c17α activity in PCOS.
Polycystic ovarian disease: US features in 104 patients.
TL;DR: The most important feature of PCOD on US scans is the bilaterally increased numbers of developing follicles, usually more than five in each ovary.
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