Effects of prenatal and lactation nicotine exposure on glucose homeostasis, lipogenesis and lipid metabolic profiles in mothers and offspring.

There is increasing evidence suggesting that maternal nicotine (NIC) exposure alone can lead to many deleterious consequences in the fetus. In this study, we aimed to evaluate the effects of prenatal and lactation NIC exposure on glucose homeostasis, lipogenesis and lipid metabolism in mothers and pups. After maternal NIC exposure (from gestational day 9 to weaning), NIC mothers showed lower body weight, decreased parametrial white adipose tissue (pWAT) and inguinal WAT weights, lower homeostasis model assessment of beta cell function, higher serum total cholesterol (TC) and low-density lipoprotein cholesterol levels, higher Castelli index values, lower hepatic mRNA levels of sterol regulatory element binding protein-1c (SREBP1c), lipoprotein lipase, acetyl-CoA carboxylase, fatty acid synthase (FAS) and glucose transporters 4 (GLUT4), as well as lower SREBP1c, FAS, leptin and GLUT4 mRNA levels in pWAT. However, female NIC pups presented higher body weights and serum TC levels, and increased trends for high density lipoprotein-cholesterol and Castelli index I. Male NIC pups had higher body weight, serum TC levels and Castelli index I values, and lower glycemia levels. Additionally, hepatic and adipose FAS gene expression from the female NIC pups presented a decreasing trend, while the male NIC pups had lower hepatic FAS expression and higher adipose FAS expression. In conclusion, prenatal and lactation NIC exposure induced deleterious effects on the glucose homeostasis, lipogenesis and lipid metabolism in both mothers and pups, which may promote several important metabolic disorders in the progeny. Additionally, there are gender-specific effects on pups.