Maternal obesity increases the risk of obesity in offspring, and obesity is accompanied by an increase in blood leptin levels. The "yellow" mutation at the mouse agouti locus (Ay) increases blood leptin levels in C57Bl pre-obese pregnant mice without affecting other metabolic characteristics. We investigated the influence of the Ay mutation or leptin injection at the end of pregnancy in C57Bl mice on metabolic phenotypes and the susceptibility to diet-induced obesity (DIO) in offspring. In both C57Bl-Ay and leptin-treated mice, the maternal effect was more pronounced in male offspring. Compared to males born to control mothers, males born to Ay mothers displayed equal food intake (FI) but decreased body weight (BW) gain after weaning, equal glucose tolerance, enhanced FI/BW ratios on the standard diet but the same FI and BW on the high-fat diet. Males born to Ay mothers were less responsive to the anorectic effect of exogenous leptin and less resistant to fasting (were not hyperphagic and gained less weight during re-feeding after food deprivation) compared to males born to control mothers. However, all progeny displayed equal hypothalamic expression of AgRP, NPY and POMC and equal plasma leptin and glucose levels after food deprivation. Leptin injections to C57Bl mice on day 17 of pregnancy decreased BW in both male and female offspring but inhibited the FI and DIO only in male offspring. Our results show that hyperleptinemia during pregnancy has gender-specific long-term effects on energy balance regulation in progeny and does not predispose offspring to developing obesity.
- high-fat diet
- developmental programming
- Copyright © 2013, American Journal of Physiology - Regulatory, Integrative and Comparative Physiology