Allyl isothiocyanate ameliorates insulin resistance through the regulation of mitochondrial function |
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| Institution: | 1. Metabolism and Nutrition Research Group, Korea Food Research Institute, Seoungnam, Korea;2. Division of Food Biotechnology, Korea University of Science and Technology, Daejeon, Korea;1. Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, College of Life Science and Technology, Huazhong Agricultural University, Wuhan 430070, PR China;2. Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, AL 35294, USA;3. College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471003, Henan, PR China;4. Department of Physics and Materials Science, Center of Super-Diamond and Advanced Films (COSDAF), City University of Hong Kong, Hong Kong SAR, China;1. Skeletal Muscle Laboratory, University College, Kurukshetra University, Kurukshetra, Haryana 136119, India;2. Department of Microbiology, Center for Free Radical Biology, University of Alabama, Birmingham 35205, USA;3. Department of Biotechnology, All India Institute of Medical Sciences, New Delhi 110029, India;4. CSIR-Institute of Microbial Technology, Sector 39A, Chandigarh 160036, India;5. Biotechnology Department, UIET, Kurukshetra University, Kurukshetra, Haryana 136119, India |
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| Abstract: | Mitochondrial dysfunction is associated with the pathophysiology of insulin resistance. Allylisothiocyanate (AITC) is found in many cruciferous vegetables and has been reported to possess anticancer activity. However, the effect of AITC on insulin resistance and mitochondrial function has not yet been investigated. Here, we show that AITC increased glucose uptake in insulin-resistant C2C12 myotubes and augmented glucose transporter 4 (GLUT4) translocation in L6-GLUT4myc cells. AITC recovered the impaired insulin signaling evoked by free fatty acid exposure and increased mitochondrial membrane potential and mitochondrial DNA content. AITC also elevated the rate of oxygen consumption in C2C12 cells. Furthermore, mice that were fed a high-fat diet with AITC for 10 weeks had reduced diet-induced obesity and hepatic steatosis. AITC also inhibited the hyperglycemia and hyperinsulinemia induced by the consumption of a high-fat diet. Glucose and insulin tolerance tests indicated that AITC improved both glucose tolerance and insulin sensitivity. In addition, AITC inhibited hepatic gluconeogenesis and ameliorated high fat diet-induced mitochondrial dysfunction. Collectively, these data suggest that the protective effect of AITC on insulin resistance is partly mediated through the modulation of mitochondrial dysfunction. |
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