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

Content Provider	Springer Nature Link
Author	Qin, Zhen Ying Zhang, Min Guo, Xi Rong Wang, Yu Mei Zhu, Guan Zhong Ni, Yu Hui Zhao, Ya Ping Qiu, Jie Kou, Chun Zhao Qin, Rui Cao, Xin Guo
Copyright Year	2012
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.
Starting Page	579
Ending Page	586
Page Count	8
File Format	PDF
ISSN	0145479X
Journal	Journal of Bioenergetics and Biomembranes
Volume Number	44
Issue Number	5
e-ISSN	15736881
Language	English
Publisher	Springer US
Publisher Date	2012-07-22
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	α-LA LYRM1 Mitochondrial dysfunction Insulin resistance Obesity Organic Chemistry Animal Anatomy / Morphology / Histology Biochemistry Bioorganic Chemistry Animal Biochemistry
Content Type	Text
Resource Type	Article
Subject	Cell Biology Physiology

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