title: α-Lipoic acid ameliorates impaired glucose uptake in LYRM1 overexpressing 3T3-L1 adipocytes through the IRS-1/Akt signaling pathway.
abstract: Overexpression of the Homo sapiens LYR motif containing 1 (LYRM1) causes mitochondrial dysfunction and induces insulin resistance in 3T3-L1 adipocytes. α-Lipoic acid (α-LA), a dithiol compound with antioxidant properties, improves glucose transport and utilization in 3T3-L1 adipocytes. The aim of this study was to investigate the direct effects of α-LA on reactive oxygen species (ROS) production and insulin sensitivity in LYRM1 overexpressing 3T3-L1 adipocytes and to explore the underlying mechanism. Pretreatment with α-LA significantly increased both basal and insulin-stimulated glucose uptake and insulin-stimulated GLUT4 translocation, while intracellular ROS levels in LYRM1 overexpressing 3T3-L1 adipocytes were decreased. These changes were accompanied by a marked upregulation in expression of insulin-stimulated tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt following treatment with α-LA. These results indicated that α-LA protects 3T3-L1 adipocytes from LYRM1-induced insulin resistance partially via its capacity to restore mitochondrial function and/or increase phosphorylation of IRS-1 and Akt.
authors: The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
authors: Zhen-Ying
authors: ZY
authors: Qin
authors: Min
authors: M
authors: Zhang
authors: Xi-Rong
authors: XR
authors: Guo
authors: Yu-Mei
authors: YM
authors: Wang
authors: Guan-Zhong
authors: GZ
authors: Zhu
authors: Yu-Hui
authors: YH
authors: Ni
authors: Ya-Ping
authors: YP
authors: Zhao
authors: Jie
authors: J
authors: Qiu
authors: Chun-Zhao
authors: CZ
authors: Kou
authors: Rui
authors: R
authors: Qin
authors: Xin-Guo
authors: XG
authors: Cao
mesh_terms: D041721:3T3-L1 Cells; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D051017:Apoptosis Regulatory Proteins / Q000096:biosynthesis* / Q000235:genetics; D015870:Gene Expression; D005947:Glucose / Q000235:genetics / Q000378:metabolism*; D051275:Glucose Transporter Type 4 / Q000235:genetics / Q000378:metabolism; D006801:Humans; D055504:Insulin Receptor Substrate Proteins / Q000235:genetics / Q000378:metabolism*; D007333:Insulin Resistance / Q000235:genetics; D051379:Mice; D010766:Phosphorylation / Q000187:drug effects / Q000235:genetics; D021381:Protein Transport / Q000187:drug effects / Q000235:genetics; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism*; D017382:Reactive Oxygen Species; D015398:Signal Transduction / Q000187:drug effects* / Q000235:genetics; D008063:Thioctic Acid / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D051017:Apoptosis Regulatory Proteins; D051275:Glucose Transporter Type 4; D055504:Insulin Receptor Substrate Proteins; C526295:Irs1 protein, mouse; C570850:LYR motif containing 1 protein, mouse; C538836:LYRM1 protein, human; D017382:Reactive Oxygen Species; C495693:Slc2a4 protein, mouse; D008063:Thioctic Acid; D051057:Proto-Oncogene Proteins c-akt; D005947:Glucose