Prenatal hyperandrogenization alters hepatic lipid metabolism in a murine PCOS model.

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

Mar del Plata

Congreso; Reunión conjunta SAIC, SAI y SAFIS 2018. LXIII Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC).; 2018

Sociedad Argentian de investigación clínica

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 different metabolic disorders such as nonalcoholic fatty liver disease (NAFLD) and metabolic syndrome.This study aimed to evaluate the effect of prenatal hyperandrogenism on the liver lipid pathways at adult life (90 days of age).Pregnant rats were injected 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 irregular ovulatory (PHov) and anovulatory (PHanov) phenotypes. We quantified by qPCR the gene expression of enzymes involved in lipogenesis (Acaca, Acacb, Fas, Scd1) and of modulators of b-oxidation (Ppara and Cpt1). We also quantified the hepatic triglyceride content by an enzymatic kit .We found that Acaca and Acacb mRNA levels were not affected in the PH groups (p>0.05). Fas and Scd1 mRNA levels were higher in the PHov phenotype than in the control group (p