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

• Published in: Journal of bioenergetics and biomembranes Vol. 44; no. 5; p. 579
• Main Authors: 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
• Format: Journal Article
• Language: English
• Published: New York Springer Nature B.V 01.10.2012
• Subjects: Glucose; Insulin resistance; Mitochondria; Obesity; Phosphorylation; Signal transduction; Translocation
• ISSN: 0145-479X; 1573-6881
• DOI: 10.1007/s10863-012-9460-1

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.[PUBLICATION ABSTRACT]