Exposure of male mice to nicotine leads to metabolic dysfunction in their male and female offspring

In this study, we investigated the effects of paternal nicotine exposure on glucose metabolism, and adipose tissue and liver transcriptomic profiles in male and female offspring. Despite no differences in body weight during early postnatal life, female offspring displayed lower fasting glucose and reduced glucose levels during glucose tolerance tests, without alterations in insulin sensitivity.

These effects were accompanied by decreased circulating insulin and upregulation of genes involved in the insulin signaling pathway in gonadal white adipose tissue (gWAT), consistent with enhanced glucose uptake capacity. In contrast, male offspring showed no overt changes in glucose tolerance or insulin sensitivity, despite reduced plasma insulin and glucagon levels. In male offspring, liver transcriptomic analyses revealed downregulation of glucagon signaling, insulin resistance, and PPARα pathways, suggesting impaired fasting adaptation and reduced hepatic catabolic capacity.