Nutritional excess during pregnancy and lactation has a negative impact on offspring phenotype. In adulthood,
obesity and
lipid overload represent factors that compromise autophagy, a process of lysosomal degradation. Despite knowledge of the impact of
obesity on autophagy, changes in offspring of obese dams have yet to be investigated. In this study, we tested the hypothesis that
maternal obesity induced by a high fat diet (HFD) modulates autophagy
proteins in the hypothalamus and liver of the offspring of mice. At birth (d0), offspring of obese dams (HFD-O) showed an increase in p62
protein and a decrease in LC3-II, but only in the liver. After weaning (d18), the offspring of HFD-O animals showed impairment of autophagy markers in both tissues compared to control offspring (SC-O). Between day 18 and day 42, both groups received a control diet and we observed that the
protein content of p62 remained increased in the livers of the HFD-O offspring. However, after 82days, we did not find any modulation in offspring autophagy
proteins. On the other hand, when the offspring of obese dams that received an HFD from day 42 until day 82 (
OH-H) were compared with the offspring from the controls that only received an HFD in adulthood (OC-H), we saw impairment in autophagy
proteins in both tissues. In conclusion, this study describes that HFD-O offspring showed early impairment of autophagy
proteins. Although the molecular mechanisms have not been explored, it is possible that changes in autophagy markers could be associated with metabolic disturbances of offspring.