α-Lipoic acid ameliorates impaired glucose uptake in LYRM1 overexpressing 3T3-L1 adipocytes through the IRS-1/Akt signaling pathway

被引：0
作者：
Zhen-Ying Qin
Min Zhang
Xi-Rong Guo
Yu-Mei Wang
Guan-Zhong Zhu
Yu-Hui Ni
Ya-Ping Zhao
Jie Qiu
Chun-Zhao Kou
Rui Qin
Xin-Guo Cao
机构：
[1] The First Affiliated Hospital with Nanjing Medical University,Institute of Pediatrics
[2] Nanjing Medical University,Department of Child Health
[3] Huaian Maternity and Child Health Hospital,Department of Clinical Laboratory
[4] The 82nd Hospital of the People’s Liberation Army,Department of Pediatrics
[5] Nanjing Maternal and Child Health Care Hospital of Nanjing Medical University,undefined
来源：
Journal of Bioenergetics and Biomembranes | 2012年 / 44卷
关键词：
α-LA; LYRM1; Mitochondrial dysfunction; Insulin resistance; Obesity;
D O I：
暂无
中图分类号：
学科分类号：
摘要：
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.
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页码：579 / 586
页数：7
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