Metformin Improves Transcription Of Insulin Mediators, In An Insulin Resistance Model Caused By Prenatal Hyperandrogenization

MARIA FLORENCIA HEBER; GISELLE ADRIANA ABRUZZESE; ALICIA BEATRIZ MOTTA

Sao Luis, Maranhao

Congreso; 5th International Symposium on Metabolic Programming and Stress & 2nd Meeting of the Ibero-American DOHaD Chapter; 2016

DOHaD

Insulin Resistance (InR) is one of the main factors that contribute to metabolic comorbidities found in women with Polycystic Ovary Syndrome (PCOS). Insulin sensitizer drugs such as metformin (Met) improve InR as well as reproductive abnormalities in PCOS. Here, we tested the effects of prenatal hyperandrogenism (PH) on the insulin signaling pathway and the effects of Met treatment during adult life. Pregnant rats were prenatally hyperandrogenizated (HA) and a Control group was obtained, offspring were euthanized at adulthood (N=80). From day 70 to 90 of age, 20 rats of each group were treated orally daily with 50 mg/kg of Met (HAM). We evaluated serum insulin and glucose levels and HOMA-IR index. Gene expression of the insulin receptor (IR), insulin substrate 1 and 2 (IRS-1, IRS-2) and glucose transporters (GLUT2 and GLUT4) was measured by qPCR in hepatic and ovarian tissue. Serum insulin, glucose levels and HOMA-IR index were higher in HA group vs Control. Met restored the levels to those of the Control group (p