Vimentin deficiency prevents high-fat diet-induced obesity and insulin resistance in mice

Seo Yeon Kim, Inyeong Kim, Wonkyoung Cho, Goo Taeg Oh, Young Mi Park

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

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.

Original languageEnglish
Pages (from-to)97-108
Number of pages12
JournalDiabetes and Metabolism Journal
Volume45
Issue number1
DOIs
StatePublished - 2021

Keywords

  • CD36 antigens
  • Glucose transporter type 4
  • Insulin resistance
  • Obesity
  • Vimentin

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