ANDROGEN EXCESS DURING PRENATAL LIFE AFFECTS HEPATIC LIPOGENESIS IN A MURINE PCOS MODEL AT ADULT LIFE

MARIA FLORENCIA HEBER; GISELLE ADRIANA ABRUZZESE; AIME FLORENCIA SILVA; ALICIA BEATRIZ MOTTA

BUENOS AIRES

Congreso; Joint Meeting of Bioscience Societies; 2017

SAIC

Prenatal androgen excess is considered as one of the main factors contributing to the development of Polycystic Ovary Syndrome (PCOS). Most of PCOS patients present hyperinsulinemia or Insulin Resistance (IR) which are associated with different metabolic disorders such as nonalcoholic fatty liver disease (NAFLD) and steatosis. In previous results, at puberal stage (60 days of age), we have shown that prenatal hyperandrogenism (PH) affects hepatic lipogenesis, thus leading to a high risk of developing steatosis.This study aimed to evaluate the effect of PH on the regulation of lipogenesis in the liver at adult life (90 days of age).Pregnant rats were hyperandrogenized with testosterone and a control group was obtained by the injection of vehicle. The prenatally hyperandrogenized (PH) female offspring (N=150) and control offspring (C, N=96) were characterized according to the estrous cycle as ovulatory (PHov) and anovulatory (PHanov) phenotypes at adult age. The gene expression of PPARg, SREBP and ChREBP (lipogenic enzyme?s modulators), PPARa (involved in b-oxidation) and chemerin (adipokine associated with IR and NAFLD disorders) were quantified by qPCR. In addition, the hepatic triglyceride content was quantified by an enzymatic kit.We found that PPARg, SREBP and ChREBP mRNA levels were lower in both phenotypes (PHov and PHanov) than in the control group (p0.05).We conclude that the alterations promoting lipogenesis observed at puberal age are not maintained at long term. Instead, at adult age, the inhibition in this pathway may be preventing the possible accumulation of hepatic triglycerides. Nevertheless further research is needed as they might be involved in energy imbalance processes.