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Review
. 2023 Feb 15:315:121385.
doi: 10.1016/j.lfs.2023.121385. Epub 2023 Jan 9.

Does maternal low-dose cadmium exposure increase the risk of offspring to develop metabolic syndrome and/or type 2 diabetes?

Saman Saedi  1 , Sara E Watson  2 , Jamie L Young  3 , Yi Tan  4 , Kupper A Wintergerst  5 , Lu Cai  6
Affiliations
Review

Does maternal low-dose cadmium exposure increase the risk of offspring to develop metabolic syndrome and/or type 2 diabetes?

Saman Saedi et al. Life Sci. .

Abstract

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.

Keywords: Cadmium; Insulin resistance; Maternal exposure; Metabolic syndrome; Offspring; Type 2 diabetes.

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Conflict of interest statement

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

Fig. 1.
Fig. 1.
Schematic illustration of the underlying mechanisms of prenatal low-dose cadmium exposure on insulin resistance and glucose tolerance/impaired glucose metabolism in various organs, resulting in T2D pathogenesis in offspring. In the pancreas, prenatal cadmium exposure causes cadmium accumulates in insulin-producing β-cells, leading to a decrease in insulin release and an increase in blood glucose in blood. Besides the direct effect of cadmium on the pancreas, this toxic metal affects glucose transport in insulin-independent (liver) and insulin-dependent tissues (adipose tissue) and impaired glucose metabolism in offspring. Reactive oxygen species (ROS). Glutathione (GSH).
Fig. 2.
Fig. 2.
Summary of the findings for how maternal exposure to low-dose cadmium during pregnancy increases the risk of offspring to develop T2D.Previous studies demonstrate that maternal exposure to low-dose cadmium via inhalation of cadmium-contained air or dietary intake result in multiple changes in different organs of embryonic and postnatal stages, responsible for the increased risk of developing T2D (citations for this summary are referred to detail description and discussion in the text).
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