title: Allyl isothiocyanate ameliorates insulin resistance through the regulation of mitochondrial function.
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.
authors.affiliation: Metabolism and Nutrition Research Group, Korea Food Research Institute, Seoungnam, Korea; Division of Food Biotechnology, Korea University of Science and Technology, Daejeon, Korea.
authors.forename: Jiyun
authors.initials: J
authors.lastname: Ahn
authors.affiliation: Metabolism and Nutrition Research Group, Korea Food Research Institute, Seoungnam, Korea.
authors.forename: Hyunjung
authors.initials: H
authors.lastname: Lee
authors.affiliation: Metabolism and Nutrition Research Group, Korea Food Research Institute, Seoungnam, Korea.
authors.forename: Sung Won
authors.initials: SW
authors.lastname: Im
authors.affiliation: Metabolism and Nutrition Research Group, Korea Food Research Institute, Seoungnam, Korea; Division of Food Biotechnology, Korea University of Science and Technology, Daejeon, Korea.
authors.forename: Chang Hwa
authors.initials: CH
authors.lastname: Jung
authors.affiliation: Metabolism and Nutrition Research Group, Korea Food Research Institute, Seoungnam, Korea; Division of Food Biotechnology, Korea University of Science and Technology, Daejeon, Korea. Electronic address: tyhap@kfri.re.kr.
authors.forename: Tae Youl
authors.initials: TY
authors.lastname: Ha
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002460:Cell Line; D002784:Cholesterol / Q000097:blood; D004272:DNA, Mitochondrial / Q000235:genetics / Q000378:metabolism; D059305:Diet, High-Fat / Q000009:adverse effects; D005227:Fatty Acids / Q000097:blood; D005234:Fatty Liver / Q000188:drug therapy; D005943:Gluconeogenesis / Q000187:drug effects; D051275:Glucose Transporter Type 4 / Q000235:genetics / Q000378:metabolism; D006943:Hyperglycemia / Q000188:drug therapy; D006946:Hyperinsulinism / Q000188:drug therapy; D007333:Insulin Resistance; D017879:Isothiocyanates / Q000494:pharmacology*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D051379:Mice; D008810:Mice, Inbred C57BL; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D018485:Muscle Fibers, Skeletal / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D018482:Muscle, Skeletal / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D009765:Obesity / Q000188:drug therapy; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D004272:DNA, Mitochondrial; D005227:Fatty Acids; D051275:Glucose Transporter Type 4; D017879:Isothiocyanates; C495693:Slc2a4 protein, mouse; D014280:Triglycerides; D002784:Cholesterol; C004471:allyl isothiocyanate
keywords: Allylisothiocyanate (AITC); Diet-induced obesity; Glucose uptake; Insulin resistance; Mitochondria