Vimentin Deficiency Prevents High-Fat Diet-Induced Obesity and Insulin Resistance in Mice
- 주제(키워드) CD36 antigens , Glucose transporter type 4 , Insulin resistance , Obesity , Vimentin
- 주제(기타) Endocrinology & Metabolism
- 설명문(일반) [Kim, SeoYeon; Kim, Inyeong; Cho, Wonkyoung; Park, Young Mi] Ewha Womans Univ, Coll Med, Dept Mol Med, Seoul, South Korea; [Oh, Goo Taeg] Ewha Womans Univ, Immune & Vasc Cell Network Res Ctr, Dept Life Sci, Natl Creat Initiat, Seoul, South Korea
- 등재 SCIE, SCOPUS, KCI등재
- 발행기관 KOREAN DIABETES ASSOC
- 발행년도 2021
- 총서유형 Journal
- URI http://www.dcollection.net/handler/ewha/000000181487
- 본문언어 영어
- Published As http://dx.doi.org/10.4093/dmj.2019.0198
초록/요약
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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