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Exp Biol Med (Maywood). 2014 Dec;239(12):1567-74. doi: 10.1177/1535370214537746. Epub 2014 Jun 5.

Metformin prevents LYRM1-induced insulin resistance in 3T3-L1 adipocytes via a mitochondrial-dependent mechanism.

Author information

1
The First Affiliated Hospital with Nanjing Medical University, Nanjing 210036, China.
2
State Key Laboratory of Reproductive Medicine, Nanjing Maternal and Child Health Hospital of Nanjing Medical University, Nanjing 210004, China.
3
Department of Child Health, Huai'an Maternity and Child Health Hospital, Huai'an 223002, China.
4
Institute of Pediatrics, Nanjing Medical University, Nanjing 210029, China.
5
The 82nd Hospital of the People's Liberation Army, Huai'an 223001, China.
6
State Key Laboratory of Reproductive Medicine, Nanjing Maternal and Child Health Hospital of Nanjing Medical University, Nanjing 210004, China xgcao@njmu.edu.cn xrguo@njmu.edu.cn.
7
Institute of Pediatrics, Nanjing Medical University, Nanjing 210029, China xgcao@njmu.edu.cn xrguo@njmu.edu.cn.

Abstract

We previously proposed that LYR motif containing 1 (LYRM1)-induced mitochondrial reactive oxygen species (ROS) production contributes to obesity-related insulin resistance. Metformin inhibits ROS production and promotes mitochondrial biogenesis in specific tissues. We assessed the effects of metformin on insulin resistance in LYRM1-over-expressing 3T3-L1 adipocytes. Metformin enhanced basal and insulin-stimulated glucose uptake and GLUT4 translocation, reduced IRS-1 and Akt phosphorylation and ROS levels, and affected the expression of regulators of mitochondrial biogenesis in LYRM1-over-expressing adipocytes. Metformin may ameliorate LYRM1-induced insulin resistance and mitochondrial dysfunction in part via a direct antioxidant effect and in part by activating the adenosine monophosphate-activated protein kinase (AMPK)-PGC1/NRFs pathway.

KEYWORDS:

LYRM1; insulin resistance; metformin; mitochondrial biogenesis

PMID:
24903160
DOI:
10.1177/1535370214537746
[Indexed for MEDLINE]

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