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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Citations
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Steven K. Malin,John P. Kirwan,Chang Ling Sia,Frank González +3 more
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TL;DR: In this article , the authors address the current knowledge about the efficacy of these nutrients in the treatment of polycystic ovary syndrome, in view of experimental and clinical studies, and present a review of the use of natural compounds such as inositols, myo- and D-chiro-inositol, alone or in combination.
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Study of ovarian morphology in high fructose fed mice
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Stephen Franks
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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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Guillermo Romero,Louis M. Luttrell,Alan D. Rogol,Konrad Zeller,Erik L. Hewlett,Joseph Larner +5 more
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