Liver injury in PCOS murine model

MARIA FLORENCIA HEBER; GISELLE ADRIANA ABRUZZESE; ALICIA BEATRIZ MOTTA

Chascomus

Congreso; XVI Jornadas Anuales de la SAB; 2014

SAB

LIVER INJURY IN A PCOS MURINE MODEL Heber MF, Abruzzese GA, Motta AB. CEFYBO-UBA-CONICET.(florencia.heber@gmail.com) Polycystic ovary syndrome (PCOS) is strongly associated with Metabolic Syndrome (MetS) that induces liver injury known as non-alcoholic fatty liver disease (NAFLD). This liver pathology is characterized by a deregulation of lipid content and an inflammatory state. PCOS etiology remains unknown but it is hypothesized that an androgen excess during gestation causes fetal programming that affects postnatal life. In our laboratory we have developed a PCOS murine model by prenatal hyperandrogenism (PH) in which we demonstrated an elevated risk of MetS development and an incipient liver injury. Our objective is to evaluate the inflammatory state and regulation of the Prostaglandin E2(PGE2) system, also involved in liver lipolysis. Pregnant Sprague Dawley rats were separated in two groups:control (C) and PH with testosterone. We evaluated, in puberal offspring, liver lipid content by histological staining, protein levels of the limiting enzyme in PGE2 synthesis, cyclooxygenase 2 (COX-2) by Western blotting and PGE2 levels by radioinmmuno assay. We found no differences on lipid liver content between C and PH groups but COX-2 and PGE2 levels decreased in PH group. We conclude that there is a depletion of the pro-inflammatory system mediated by PGE2 and COX-2 that could be repressing the development of steatohepatitis.