title: CTRP5 ameliorates palmitate-induced apoptosis and insulin resistance through activation of AMPK and fatty acid oxidation.
abstract: Lipotoxicity resulting from a high concentration of saturated fatty acids is closely linked to development of insulin resistance, as well as apoptosis in skeletal muscle. CTRP5, an adiponectin paralog, is known to activate AMPK and fatty acid oxidation; however, the effects of CTRP5 on palmitate-induced lipotoxicity in myocytes have not been investigated. We found that globular domain of CTRP5 (gCTRP5) prevented palmitate-induced apoptosis and insulin resistance in myocytes by inhibiting the activation of caspase-3, reactive oxygen species accumulation, and IRS-1 reduction. These beneficial effects of gCTRP5 are mainly attributed to an increase in fatty acid oxidation through phosphorylation of AMPK. These results provide a novel function of CTRP5, which may have preventive and therapeutic potential in management of obesity, insulin resistance, and type 2 diabetes mellitus.
authors.affiliation: Department of Biochemistry, Dongguk University College of Medicine, Gyeongju 780-714, Republic of Korea.
authors.forename: Won-Mo
authors.initials: WM
authors.lastname: Yang
authors.affiliation: Department of Biochemistry, Dongguk University College of Medicine, Gyeongju 780-714, Republic of Korea; Endocrine Channelopathy, Channelopathy Research Center, Dongguk University College of Medicine, Goyang 410-773, Republic of Korea. Electronic address: wanlee@dongguk.ac.kr.
authors.forename: Wan
authors.initials: W
authors.lastname: Lee
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000235:genetics* / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D002460:Cell Line; D005786:Gene Expression Regulation; D055504:Insulin Receptor Substrate Proteins / Q000235:genetics / Q000378:metabolism; D007333:Insulin Resistance; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism* / Q000494:pharmacology; D032342:Muscle Cells / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D009124:Muscle Proteins / Q000235:genetics / Q000378:metabolism* / Q000494:pharmacology; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D010084:Oxidation-Reduction / Q000187:drug effects; D019308:Palmitic Acid / Q000494:pharmacology*; D010766:Phosphorylation; D017434:Protein Structure, Tertiary; D051381:Rats; D017382:Reactive Oxygen Species / Q000037:antagonists & inhibitors / Q000378:metabolism; D011994:Recombinant Proteins / Q000235:genetics / Q000378:metabolism* / Q000494:pharmacology; D015398:Signal Transduction
chemical_list: C544682:C1QTNF5 protein, rat; D055504:Insulin Receptor Substrate Proteins; D047908:Intracellular Signaling Peptides and Proteins; C526296:Irs1 protein, rat; D009124:Muscle Proteins; D017382:Reactive Oxygen Species; D011994:Recombinant Proteins; D019308:Palmitic Acid; D055372:AMP-Activated Protein Kinases; C505410:Casp3 protein, rat; D053148:Caspase 3
keywords: AMPK; CTRP5; IRS-1; Insulin resistance; Palmitate