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Nutritional status during gestation may lead to a phenomenon known as metabolic programming, which can be triggered by epigenetic mechanisms. The  Let-7  family of microRNAs were one of the first to be discovered, and are closely related to metabolic processes. Bioinformatic analysis revealed that  Prkaa2 , the gene that encodes AMPK α2, is a predicted target of  Let-7 . Here we aimed to investigate whether  Let-7  has a role in AMPKα2 levels in the NAFLD development in the offspring programmed by maternal obesity.  Let-7  levels were upregulated in the liver of newborn mice from obese dams, while the levels of  Prkaa2  were downregulated.  Let-7  levels strongly correlated with serum glucose, insulin and NEFA, and in vitro treatment of AML12 with glucose and NEFA lead to higher  Let-7  expression. Transfection of  Let-7a  mimic lead to downregulation of AMPKα2 levels, while the transfection with  Let-7a  inhibitor impaired both NEFA-mediated reduction of  Prkaa2  levels and the fat accumulation driven by NEFA. The transfection of  Let-7a  inhibitor in ex-vivo liver slices from the offspring of obese dams restored phospho-AMPKα2 levels. In summary,  Let-7a  appears to regulate hepatic AMPKα2 protein levels and lead to the early hepatic metabolic disturbances in the offspring of obese dams.

MicroRNA Let-7 targets AMPK and impairs hepatic lipid metabolism in offspring of maternal obese pregnancies