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KMID : 1200020210450010097
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Diabetes & Metabolism Journal
2021 Volume.45 No. 1 p.97 ~ p.108
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Vimentin Deficiency Prevents High-Fat Diet-Induced Obesity and Insulin Resistance in Mice
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Kim Seo-Yeon
Kim In-Yeong
Cho Won-Kyoung
Oh Goo-Taeg
Park Young-Mi
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Abstract
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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.
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KEYWORD
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CD36 antigens, Glucose transporter type 4, Insulin resistance, Obesity, Vimentin
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