后代
镉
胰岛素抵抗
怀孕
代谢综合征
2型糖尿病
内分泌学
医学
生理学
内科学
糖尿病
胎儿
生物
化学
遗传学
有机化学
作者
Saman Saedi,Sara E. Watson,Jamie L. Young,Yi Tan,Kupper A. Wintergerst,Lu Cai
出处
期刊:Life Sciences
[Elsevier]
日期:2023-02-01
卷期号:315: 121385-121385
被引量:8
标识
DOI:10.1016/j.lfs.2023.121385
摘要
Cadmium is a hazardous metal with multiple organ toxicity that causes great harm to human health. Cadmium enters the human body through occupational exposure, diet, drinking water, breathing, and smoking. Cadmium accumulation in the human body is associated with increased risk of developing obesity, cardiovascular disease, diabetes, and metabolic syndrome (MetS). Cadmium uptake is enhanced during pregnancy and can cross the placenta affecting placental development and function. Subsequently, cadmium can pass to fetus, gathering in multiple organs such as the liver and pancreas. Early-life cadmium exposure can induce hepatic oxidative stress and pancreatic β-cell dysfunction, resulting in insulin resistance and glucose metabolic dyshomeostasis in the offspring. Prenatal exposure to cadmium is also associated with increasing epigenetic effects on the offspring's multi-organ functions. However, whether and how maternal exposure to low-dose cadmium impacts the risks of developing type 2 diabetes (T2D) in the young and/or adult offspring remains unclear. This review collected available data to address the current evidence for the potential role of cadmium exposure, leading to insulin resistance and the development of T2D in offspring. However, this review reveals that underlying mechanisms linking prenatal cadmium exposure during pregnancy with T2D in offspring remain to be adequately investigated.
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