Maternal obesity during pregnancy is associated with several metabolic impairments in offspring, some of them evidenced from early infancy. Some reports have demonstrated that offspring of obese rats, whose obesity was induced by high fat diet consumption, have an increase sympathetic tone and increased norepinephrine (NE) content in kidney, liver and ovary. We recently reported that maternal administration of metformin prevents the increase in ovarian NE in offspring when they are adult. Since norepinephrine signaling is like glucagon in liver, we aimed to evaluate whether hepatic gene expression of lipogenic enzymes is altered in adult offspring of obese rats and if it is associated with norepinephrine levels. Also, we evaluated whether metformin (250 mg/Kg) during pregnancy prevented the liver alterations observed in offspring of obese mothers. To achieve this, we measure norepinephrine b\.y HPLC coupled to electrochemical detection, Tyrosine hydroxylase by Western blot, and acetyl CoA carboxylase (ACC) and fatty acid synthase (FAS) by qPCR in the liver. Our results showed an increase in FAS and ACC expression in offspring of obese mothers, along with a tendency to increase in liver norepinephrine. Metformin prevented the increase in FAS and ACC expression in offspring of obese mothers but, intriguingly, it increased TH expression and norepinephrine levels both in offspring of obese and offspring of control rats. In conclusion, metformin prevented the alterations in the expression of lipogenic enzymes induced by maternal obesity during pregnancy but altered the sympathetic control of the liver.
18 - 21 May 2019
European Society of Endocrinology