Moroni-González Diana, Sarmiento-Ortega Victor Enrique, Diaz Alfonso, Brambila Eduardo, Treviño Samuel
Laboratory of Chemical-Clinical Investigations, Department of Clinical Chemistry, Faculty of Chemistry Science, Meritorious Autonomous University of Puebla, Ciudad Universitaria, Puebla 72560, Mexico.
Department of Pharmacy, Faculty of Chemistry Science, Meritorious Autonomous University of Puebla, 22 South. FCQ9, Ciudad Universitaria, Puebla 72560, Mexico.
Toxics. 2023 Feb 26;11(3):223. doi: 10.3390/toxics11030223.
Cadmium has been well recognized as a critical toxic agent in acute and chronic poisoning cases in occupational and nonoccupational settings and environmental exposure situations. Cadmium is released into the environment after natural and anthropogenic activities, particularly in contaminated and industrial areas, causing food pollution. In the body, cadmium has no biological activity, but it accumulates primarily in the liver and kidney, which are considered the main targets of its toxicity, through oxidative stress and inflammation. However, in the last few years, this metal has been linked to metabolic diseases. The pancreas-liver-adipose axis is largely affected by cadmium accumulation. Therefore, this review aims to collect bibliographic information that establishes the basis for understanding the molecular and cellular mechanisms linked to cadmium with carbohydrate, lipids, and endocrine impairments that contribute to developing insulin resistance, metabolic syndrome, prediabetes, and diabetes.
镉在职业和非职业环境以及环境暴露情况下的急慢性中毒案例中，已被公认为一种关键的有毒物质。镉在自然和人为活动后释放到环境中，尤其是在受污染地区和工业区，导致食物污染。在体内，镉没有生物活性，但它主要通过氧化应激和炎症作用，在肝脏和肾脏中蓄积，而肝脏和肾脏被认为是其毒性的主要靶器官。然而，在过去几年中，这种金属已与代谢性疾病相关联。胰腺 - 肝脏 - 脂肪轴在很大程度上受到镉蓄积的影响。因此，本综述旨在收集文献信息，为理解与镉相关的分子和细胞机制奠定基础，这些机制涉及碳水化合物、脂质和内分泌功能障碍，进而导致胰岛素抵抗、代谢综合征、糖尿病前期和糖尿病的发生。
