The pervasive impact of obesity across generations is one of our most serious public health concerns. Having either parent obese is an independent risk factor for childhood obesity. It is now clear that both maternal and paternal factors play key roles via non-genetic mechanisms. Given the intractable nature of obesity on a global scale, one of the key interests of our lab is determining ways of ameliorating the impact of obesity in parents on the next generation using relevant rodent models. While male obesity is associated with impaired sperm function and increased sperm DNA damage, there is increasing evidence for adverse impacts on offspring metabolic function.
Detrimental impacts of maternal obesity on offspring adiposity, metabolism and cardiovascular risk are well established. Maternal obesity is also a major risk factor for negative maternal and infant outcomes. In rat the impact of maternal obesity was reduced by postweaning voluntary exercise in offspring, with greater benefits observed in those who were more compromised due to post-weaning high fat diet consumption. We next tested effects of exercise in obese mothers during pregnancy; significant metabolic benefits were observed, even though little impact was discernible in the mother. Experiments in mice compared the impact of treadmill exercise and the NAD+ precursor NMN, on oocyte gene expression. Thus rodent studies offer a great opportunity to test proof of concept of novel interventions to improve fertility. Given the marked increase in obesity, reversing its influence on the germ line warrants special consideration.