| First Author | Kim S | Year | 2020 |
| Journal | Diabetes Metab J | PubMed ID | 32602277 |
| Mgi Jnum | J:298201 | Mgi Id | MGI:6477433 |
| Doi | 10.4093/dmj.2019.0198 | Citation | Kim S, et al. (2020) Vimentin Deficiency Prevents High-Fat Diet-Induced Obesity and Insulin Resistance in Mice. Diabetes Metab J |
| abstractText | BACKGROUND: Obesity and type 2 diabetes mellitus are world-wide health problems, and lack of understanding of their linking mechanism is one reason for limited treatment options. We determined if genetic deletion of vimentin, a type 3 intermediate filament, affects obesity and type 2 diabetes mellitus. METHODS: We fed vimentin-null (Vim(-/-)) mice and wild-type mice a high-fat diet (HFD) for 10 weeks and measured weight change, adiposity, blood lipids, and glucose. We performed intraperitoneal glucose tolerance tests and measured CD36, a major fatty acid translocase, and glucose transporter type 4 (GLUT4) in adipocytes from both groups of mice. RESULTS: Vim(-/-) mice fed an HFD showed less weight gain, less adiposity, improved glucose tolerance, and lower serum level of fasting glucose. However, serum triglyceride and non-esterified fatty acid levels were higher in Vim(-/-) mice than in wild-type mice. Vimentin-null adipocytes showed 41.1% less CD36 on plasma membranes, 27% less uptake of fatty acids, and 50.3% less GLUT4, suggesting defects in intracellular trafficking of these molecules. CONCLUSION: We concluded that vimentin deficiency prevents obesity and insulin resistance in mice fed an HFD and suggest vimentin as a central mediator linking obesity and type 2 diabetes mellitus. |
