Correlation Engine 2.0
Clear Search sequence regions

Sizes of these terms reflect their relevance to your search.

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. Copyright © 2022 Elsevier Ltd. All rights reserved.


Bo He, Qi Zhang, Yu Guo, Ying Ao, Kai Tie, Hao Xiao, Liaobin Chen, Dan Xu, Hui Wang. Prenatal smoke (Nicotine) exposure and offspring's metabolic disease susceptibility in adulthood. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association. 2022 Oct;168:113384

Expand section icon Mesh Tags

Expand section icon Substances

PMID: 36041661

View Full Text