SeoYeon Kim1, Inyeong Kim1, Wonkyoung Cho1, Goo Taeg Oh2, Young Mi Park3. 1. Department of Molecular Medicine, College of Medicine, Ewha Womans University, Seoul, Korea. 2. Immune and Vascular Cell Network Research Center, National Creative Initiatives, Department of Life Sciences, Ewha Womans University, Seoul, Korea. 3. Department of Molecular Medicine, College of Medicine, Ewha Womans University, Seoul, Korea. parkym@ewha.ac.kr.
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.
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.
Authors: Seo Yeon Kim; Se-Jin Jeong; Ji-Hae Park; Wonkyoung Cho; Young-Ho Ahn; Youn-Hee Choi; Goo Taeg Oh; Roy L Silverstein; Young Mi Park Journal: Front Cardiovasc Med Date: 2022-05-18
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Authors: Tamara Camino; Nerea Lago-Baameiro; Aurelio Sueiro; Susana Belén Bravo; Iván Couto; Francisco Fernando Santos; Javier Baltar; Felipe F Casanueva; María Pardo Journal: Int J Mol Sci Date: 2022-09-16 Impact factor: 6.208