Cadmium (Cd) is a heavy metal that acts as endocrine disrupting chemical (EDC). Few studies have investigated the effects of Cd exposure on metabolic dysfunctions, such as type 1 and 2 diabetes mellitus (T1DM and T2DM). Thus, we assessed whether subacute Cd exposure at occupational levels causes abnormalities in white adipose tissue (WAT), liver, pancreas, and skeletal muscle. We administered cadmium chloride (CdCl2) (100 ppm in drinking water for 30 days) to female rats and evaluated Cd levels in serum and metabolic organs, morphophysiology, inflammation, oxidative stress, fibrosis, and gene expression. High Cd levels were found in serum, WAT, liver, pancreas, and skeletal muscle. Cd‐exposed rats showed low adiposity, dyslipidemia, insulin resistance, systemic inflammation, and oxidative stress compared to controls. Cd exposure reduced adipocyte size, hyperleptinemia, increased cholesterol levels, inflammation, apoptosis and fibrosis in WAT. Cd‐exposed rats had increased liver cholesterol levels, insulin receptor beta (IRβ) and peroxisome proliferator‐activated receptor‐gamma coactivator‐1alpha (PGC1α) expression, karyomegaly, inflammation, and fibrosis. Cd exposure reduced insulin levels and pancreatic islet size and increased inflammation and fibrosis. Cd exposure reduced skeletal muscle fiber diameter and increased IR expression and inflammation. Finally, strong positive correlations were observed between serum, tissue Cd levels, abnormal morphology, tissue inflammation and fibrosis. Thus, these data suggest that subacute Cd exposure impairs WAT, liver, pancreas and skeletal muscle function, leading to T1DM and T2DM features and other complications in female rats.

中文翻译：

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亚急性镉暴露改变不同的代谢功能，导致雌性大鼠出现1型和2型糖尿病特征

镉 (Cd) 是一种重金属，具有内分泌干扰化学物质 (EDC) 的作用。很少有研究调查镉暴露对代谢功能障碍的影响，例如 1 型和 2 型糖尿病（T1DM 和 T2DM）。因此，我们评估了职业水平的亚急性镉暴露是否会导致白色脂肪组织（WAT）、肝脏、胰腺和骨骼肌异常。我们施用氯化镉（CdCl2）（饮用水中 100 ppm，持续 30 天）给雌性大鼠，并评估血清和代谢器官、形态生理学、炎症、氧化应激、纤维化和基因表达中的镉水平。血清、WAT、肝脏、胰腺和骨骼肌中镉含量较高。与对照组相比，暴露于镉的大鼠表现出较低的肥胖、血脂异常、胰岛素抵抗、全身炎症和氧化应激。镉暴露减少了 WAT 中的脂肪细胞大小、高瘦素血症、胆固醇水平升高、炎症、细胞凋亡和纤维化。暴露于镉的大鼠肝脏胆固醇水平升高，胰​​岛素受体β（IRβ）和过氧化物酶体增殖物激活受体-γ共激活剂-1α（PGC1α）表达增加，并出现核肿大、炎症和纤维化。镉暴露降低了胰岛素水平和胰岛大小，并增加了炎症和纤维化。镉暴露减少了骨骼肌纤维直径并增加了 IR 表达和炎症。最后，观察到血清、组织镉水平、异常形态、组织炎症和纤维化之间存在强正相关性。因此，这些数据表明，亚急性镉暴露会损害 WAT、肝脏、胰腺和骨骼肌功能，导致雌性大鼠出现 T1DM 和 T2DM 特征以及其他并发症。