microRNA-130 and microRNA-122 alteration are related to lipid metabolic impairments in the foetal liver of rats with gestational diabetes mellitus

D. FORNES, V. WHITE, F. HEINECKE, E. CAPOBIANCO, A. JAWERBAUM.; D. FORNES, V. WHITE, F. HEINECKE, E. CAPOBIANCO, A. JAWERBAUM.

Puerto Varas

Congreso; VII SLIMP Latin American Symposium on Maternal Fetal Interaction and Placenta; 2017

Gestational diabetes mellitus (GDM) is a prevalent disease that increases the risk of adverse foetal outcomes. MicroRNA-130 (miR-130) targets the nuclear receptor PPAR, a master regulator of lipid metabolism. MicroRNA-122 (miR-122), the most abundant microRNA in the liver, regulates hepatocyte differentiation and metabolism. Fatty acid synthase (FAS) is a target gene of both PPAR and miR-122. Objectives: Aiming to find putative lipid liver anomalies we analyzed miR-130, miR-122, PPAR, FAS expression, and triglyceride content in the foetal liver in a novel model of GDM in the rat. Methods: GDM was spontaneously induced by intrauterine programming in the offspring (F1) of diabetic rats (F0 diabetic rats were obtained through neonatal streptozotocin administration (90 mg/Kg), glycaemia values (180-230 mg/dl) significantly higher from controls values (80-100 mg/dl)). In control and GDM rats, livers of male foetuses were explanted on day 21 of gestation, miR-130, miR-122, and FAS analyzed by qPCR, PPAR by Western blot, and triglyceride content by thin-layer chromatography. Results: Foetal livers from GDM rats showed reduced miR-130 (52%, P