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Maternal obesity induced by high fat diet (HFD) during pregnancy and lactation.can negatively interfere in the development of offspring. In adulthood, obesity and lipid overload represent factors that compromise autophagy, a process of lysosomal degradation that is essential for the maintenance of cellular homeostasis. Based in this context, the aim of this study was to evaluate the protein content of LC3-II, a principal marker of cellular autophagy, in the hypothalamus and liver of offspring at birth, after weaning and in adulthood. At birth, the offspring showed a decrease of LC3-II protein content only in the liver of offspring from obese dams (HFD-O) when compared to offspring control (SC-O). At weaning LC3-II decreased in both hypothalamic and hepatic tissue. However, during adulthood there were no differences between the groups. Overall, we believe that this study demonstrates that offspring’s LC3-II, as well as in adulthood, is also highly associated with exposure to lipids and obesity.

Modulation of protein content of LC3-II in offspring of animals submitted to the high fat diet during intrauterine life and lactation