Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/57377
Title: Prolonged fasting elicits increased hepatic triglyceride accumulation in rats born to dexamethasone-treated mothers
Authors: Pantaleao, Lucas Carminatti
Murata, Gilson
Teixeira, Caio Jordao
Payolla, Tanyara Baliani
Santos-Silva, Junia Carolina
Duque-Guimaraes, Daniella Esteves
Sodre, Frhancielly S.
Lellis-Santos, Camilo [UNIFESP]
Vieira, Juliana Camargo
de Souza, Dailson Nogueira
Gomes, Patricia Rodrigues
Rodrigues, Sandra Campos
Anhe, Gabriel Forato
Bordin, Silvana
Issue Date: 2017
Publisher: Nature Publishing Group
Citation: Scientific Reports. London, v. 7, p. -, 2017.
Abstract: We investigated the effect of dexamethasone during the last week of pregnancy on glucose and lipid metabolism in male offspring. Twelve-week old offspring were evaluated after fasting for 12-hours (physiological) and 60-hours (prolonged). Physiological fasting resulted in glucose intolerance, decreased glucose clearance after pyruvate load and increased PEPCK expression in rats born to dexamethasone-treated mothers (DEX). Prolonged fasting resulted in increased glucose tolerance and increased glucose clearance after pyruvate load in DEX. These modulations were accompanied by accumulation of hepatic triglycerides (TG). Sixty-hour fasted DEX also showed increased citrate synthase (CS) activity, ATP citrate lyase (ACLY) content, and pyruvate kinase 2 (pkm2), glucose transporter 1 (slc2a1) and lactate dehydrogenase-a (ldha) expressions. Hepatic AKT2 was increased in 60-hour fasted DEX, in parallel with reduced miRNAs targeting the AKT2 gene. Altogether, we show that metabolic programming by prenatal dexamethasone is characterized by an unexpected hepatic TG accumulation during prolonged fasting. The underlying mechanism may depend on increased hepatic glycolytic flux due to increased pkm2 expression and consequent conversion of pyruvate to non-esterified fatty acid synthesis due to increased CS activity and ACLY levels. Upregulation of AKT2 due to reduced miRNAs may serve as a permanent mechanism leading to increased pkm2 expression.
URI: https://repositorio.unifesp.br/handle/11600/57377
ISSN: 2045-2322
Other Identifiers: http://dx.doi.org/10.1038/s41598-017-10642-1
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