Tributyltin exposure disturbs hepatic glucose metabolism in male mice
| Autor: | Binshui Li, Kunlin Ou, Jing Xu, Zhenghong Zuo, Chonggang Wang, Jiaojiao Guo, Chuqiao Chen |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Male
0301 basic medicine medicine.medical_specialty Blotting Western Fluorescent Antibody Technique Real-Time Polymerase Chain Reaction Toxicology Glucagon Mice 03 medical and health sciences 0302 clinical medicine Insulin resistance Hyperinsulinism Insulin-Secreting Cells Internal medicine Diabetes mellitus Glucose Intolerance Receptors Glucagon medicine Animals Glucose homeostasis Chemistry Increased hepatic glycogen content Gluconeogenesis Glucose Tolerance Test medicine.disease Glucose 030104 developmental biology Endocrinology Liver Glucagon-Secreting Cells Trialkyltin Compounds Phosphoenolpyruvate carboxykinase Glucagon receptor 030217 neurology & neurosurgery |
| Zdroj: | Toxicology. 425:152242 |
| ISSN: | 0300-483X |
| DOI: | 10.1016/j.tox.2019.152242 |
| Popis: | Some previous studies showed that organotin compounds induced diabetes in animal models. The underlying mechanisms should be further revealed. In this study, male KM mice were exposed to tributyltin (TBT) at 0.5, 5 and 50 μg/kg once every three days for 45 days. The TBT-treated mice exhibited an elevation of fasting blood glucose level and glucose intolerance. The fasting serum insulin levels were increased and reached a significant difference in the 50 μg/kg group; the glucagon levels were significantly decreased in all the treatments. Pancreatic β-cell mass was significantly decreased in all the treatments; α-cell mass showed a significant decrease in the 5 and 50 ug/kg groups. The transcription of pancreatic insulin gene (Ins2) showed an up-regulation and reached a significant difference in the 5 and 50 μg/kg groups, which would be responsible for the increased serum insulin levels. The transcription of glucagon gene (Gcg) in the pancreas was significantly down-regulated in the 5 and 50 ug/kg groups. The protein expression of hepatic glucagon receptor was down-regulated, while the expression of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase was up-regulated accompanied by increased hepatic glycogen content. These results indicated that hepatic gluconeogenesis was enhanced during insulin resistance stage caused by TBT exposure, which would exert a potential risk inducing the development of diabetes mellitus. |
| Databáze: | OpenAIRE |
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