AI Article Synopsis
- Metformin (MET) is a common medication for type 2 diabetes that's now being studied in younger patients, particularly those where Sertoli cells are still growing.
- The study aims to explore how MET affects the way follicle-stimulating hormone (FSH) influences Sertoli cell growth, focusing on molecular mechanisms in eight-day-old rat cultures.
- Findings indicate that MET reduces the proliferation of Sertoli cells stimulated by FSH and alters related molecular signals, suggesting it can counteract FSH's effects on these cells' growth.
Article Abstract
Metformin (MET) is one of the most widely used anti-hyperglycemic agents for treating patients with type 2 diabetes and it has started to be used in pediatric population at ages when Sertoli cells are still proliferating. It is well known that follicle-stimulating hormone (FSH) is the major Sertoli cell mitogen. The aim of the study is to investigate a possible effect of MET, which has been shown to have anti-proliferative properties, on FSH regulation of postnatal Sertoli cell proliferation and on the molecular mechanisms involved in this regulation. The present study was performed in eight-day-old rat Sertoli cell cultures. The results obtained show that MET in the presence of FSH increases phosphorylated acetyl-CoA carboxylase and decreases phosphorylated p70S6K levels. Moreover, we show that MET decreases FSH-stimulated Sertoli cell proliferation, and this decrease is accompanied by a reduction in FSH-stimulated and expression and an increase in cell cycle inhibitor expression. Altogether, these results suggest that MET can, at least in part, counteract the effect of FSH on postnatal Sertoli cell proliferation.
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| http://dx.doi.org/10.1530/REP-18-0233 | DOI Listing |
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