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Vimentin Deficiency Prevents High-Fat Diet-Induced Obesity and Insulin Resistance in Mice

Title
Vimentin Deficiency Prevents High-Fat Diet-Induced Obesity and Insulin Resistance in Mice
Authors
Kim, SeoYeonKim, InyeongCho, WonkyoungOh, Goo TaegPark, Young Mi
Ewha Authors
오구택박영미조원경
SCOPUS Author ID
오구택scopus; 박영미scopus; 조원경scopusscopus
Issue Date
2021
Journal Title
DIABETES & METABOLISM JOURNAL
ISSN
2233-6079JCR Link

2233-6087JCR Link
Citation
DIABETES & METABOLISM JOURNAL vol. 45, no. 1, pp. 97 - +
Keywords
CD36 antigensGlucose transporter type 4Insulin resistanceObesityVimentin
Publisher
KOREAN DIABETES ASSOC
Indexed
SCIE; SCOPUS; KCI WOS
Document Type
Article
Abstract
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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DOI
10.4093/dmj.2019.0198
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자연과학대학 > 생명과학전공 > Journal papers
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