TY - JOUR
T1 - Vimentin deficiency prevents high-fat diet-induced obesity and insulin resistance in mice
AU - Kim, Seo Yeon
AU - Kim, Inyeong
AU - Cho, Wonkyoung
AU - Oh, Goo Taeg
AU - Park, Young Mi
N1 - Funding Information:
This work was supported by a National Research Foundation of Korea (NRF) grant funded by the Korean government (MSIP)(No. NRF-2015M3A9B6029133) and was partly supported by a grant funded by Health Fellowship Foundation.
Publisher Copyright:
© 2021 Korean Diabetes Association
PY - 2021
Y1 - 2021
N2 - 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.
AB - 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.
KW - CD36 antigens
KW - Glucose transporter type 4
KW - Insulin resistance
KW - Obesity
KW - Vimentin
UR - http://www.scopus.com/inward/record.url?scp=85101896572&partnerID=8YFLogxK
U2 - 10.4093/DMJ.2019.0198
DO - 10.4093/DMJ.2019.0198
M3 - Article
C2 - 32602277
AN - SCOPUS:85101896572
SN - 2233-6079
VL - 45
SP - 97
EP - 108
JO - Diabetes and Metabolism Journal
JF - Diabetes and Metabolism Journal
IS - 1
ER -