Effects of in utero androgen excess and metformin treatment on hepatic functions

This study aimed to evaluate the role of prenatal hyperandrogenization in liver functions and the extent of metformin as treatment. Pregnant rats were hyperandrogenized with subcutaneous testosterone (1mg/rat) between 16 and 19 of pregnancy. Prenatally hyperandrogenized (PH) female offspring display...

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Bibliographic Details
Authors: Abruzzese, Giselle Adriana, Heber, María Florencia, Ferrer, María José, Ferreira, Silvana Rocio, Silva, Aimé Florencia, Motta, Alicia Beatriz
Format: article
Status:Published version
Publication Date:2019
Country:Argentina
Institution:Consejo Nacional de Investigaciones Científicas y Técnicas
Repository:CONICET Digital (CONICET)
Language:English
OAI Identifier:oai:ri.conicet.gov.ar:11336/120109
Online Access:http://hdl.handle.net/11336/120109
Access Level:Open access
Keyword:Prenatal hyperandogenization
Liver function
Metformin treatment
https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
Description
Summary:This study aimed to evaluate the role of prenatal hyperandrogenization in liver functions and the extent of metformin as treatment. Pregnant rats were hyperandrogenized with subcutaneous testosterone (1mg/rat) between 16 and 19 of pregnancy. Prenatally hyperandrogenized (PH) female offspring displayed, at the adult life, two phenotypes; a PH irregular ovulatory phenotype (PHiov) and a PH anovulatory (PHanov) phenotype. From day 70 to the moment of sacrifice (90 days of age), 50% of the animals of each group received a daily oral dose of 50 mg/kg of metformin. We found that both PH phenotypes displayed a hepatic disruptions of insulin and glucose pathway and that metformin treatment reversed some of these alterations in a specific-phenotype manner. Our findings show, for the first time, that androgen excess in utero promotes hepatic dysfunctions and that metformin treatment is able to specifically reverse those hepatic alterations and sheds light on the possible mechanisms of metformin action.