Prenatal smoke (Nicotine) exposure and offspring's metabolic disease susceptibility in adulthood.

Abstract

Exposure to smoking (nicotine) during pregnancy not only directly affects fetal development, but also increases susceptibility to metabolic diseases in adulthood, but the mechanism of action remains unclear. Here, we review epidemiological and laboratory studies linking these relationships. In addition to the direct effect of nicotine on the fetus, intrauterine neuroendocrine-metabolic programming mediated by maternal glucocorticoid overexposure also plays an important role, involving glucocorticoid-insulin-like growth factor 1 (GC-IGF1) axis, hypothalamic-pituitary-adrenal (HPA) axis, renin-angiotensin system (RAS) and other endocrine systems. Epigenetics is involved in intrauterine neuroendocrine-metabolic programming, metabolic disease susceptibility and multigenerational inheritance. There are "two programming" and "two strikes" mechanisms for the occurrence of fetal-originated metabolic diseases in adulthood. These innovative research summaries and academic viewpoints provide experimental and theoretical basis for systematically elucidating the occurrence and development of fetal-originated metabolic diseases.