ArticleEndocrine2022
Cadmium exposure decreases fasting blood glucose levels and exacerbates type-2 diabetes in a mouse model.
Article in Endocrine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Metals in the human liver: An underappreciated risk factor of hepatic insulin resistance and associated pathophysiology.Environmental pollution (Barking, Essex : 1987) · 2025Review
- Environmental cadmium exposure aggravates renal fibrosis and reduced renal lipid accumulation in diabetic mice.Lipids in health and disease · 2025Article
- Evaluation of cadmium effects on the glucose metabolism on insulin resistance HepG2 cells.Heliyon · 2024Article
- Integrating Transcriptomics and Proteomics to Characterize the Intestinal Responses to Cadmium Exposure Using a Piglet Model.International journal of molecular sciences · 2024Article
- TAK-242 alleviates diabetic cardiomyopathy via inhibiting pyroptosis and TLR4/CaMKII/NLRP3 pathway.Open life sciences · 2024Article
- Potential pathogenic roles of ferroptosis and cuproptosis in cadmium-induced or exacerbated cardiovascular complications in individuals with diabetes.Frontiers in endocrinology · 2024Review
- Proteomic analysis of vitreal exosomes in patients with proliferative diabetic retinopathy.Eye (London, England) · 2023Article
- SXRF for Studying the Distribution of Trace Metals in the Pancreas and Liver.Antioxidants (Basel, Switzerland) · 2023Article
- Does maternal low-dose cadmium exposure increase the risk of offspring to develop metabolic syndrome and/or type 2 diabetes?Life sciences · 2023Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeAlthough the effects of cadmium (Cd) on the development of diabetes have been extensively investigated, the relationship between Cd exposure and the severity of established diabetes is unclear. Herein, we investigate the effects of long-term exposure to Cd in a streptozotocin-induced mouse model of type-2 diabetes mellitus (T2DM) and the underlying mechanism.
methodsC57BL/6 Mice were divided into the following four groups: (1) control group; (2) Cd-exposed group; (3) diabetic group; (4) Cd-exposed diabetic group. Cd exposure was established by the administration of 155 ppm CdCl
resultsClinical signs attributable to diabetes were more apparent in Cd-exposed diabetic mice, while no effects of Cd exposure were found on non-diabetic mice. Cd exposure significantly decreased fasting blood glucose (FBG) levels in diabetic group. We further demonstrated that the glycolysis related hepatic enzymes, pyruvate kinase M2 (PKM-2) and lactic dehydrogenase A (LDHA) were both increased, while the gluconeogenesis related hepatic enzymes, phosphoenolpyruvate-1 (PCK-1) and glucose-6-phosphatase (G6Pase) were both decreased in Cd exposed diabetic mice, indicating that Cd increased glycolysis and inhibited gluconeogenesis in diabetic model. Moreover, lactate accumulation was noted accompanied by the increased inflammation and fibrosis in the livers of diabetic mice following Cd exposure.
conclusionsCd exposure disturbed glucose metabolism and exacerbated diabetes, providing a biological relevance that DM patients are at greater risk when exposed to Cd.
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