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.

怀孕期间接触吸烟（尼古丁）不仅直接影响胎儿发育，还会增加成年期对代谢疾病的易感性，但作用机制尚不清楚。在这里，我们回顾了将这些关系联系起来的流行病学和实验室研究。除了尼古丁对胎儿的直接影响外，母体糖皮质激素过度暴露介导的宫内神经内分泌代谢程序也起着重要作用，涉及糖皮质激素-胰岛素样生长因子 1 (GC-IGF1) 轴、下丘脑-垂体-肾上腺。 HPA) 轴、肾素-血管紧张素系统 (RAS) 和其他内分泌系统。表观遗传学涉及宫内神经内分泌代谢编程、代谢疾病易感性和多代遗传。成年期胎儿源性代谢疾病的发生有“两次编程”和“两次打击”机制。这些创新的研究总结和学术观点为系统阐明胎儿源性代谢疾病的发生发展提供了实验和理论依据。