NDLI: Silencing miR-106b improves palmitic acid-induced mitochondrial dysfunction and insulin resistance in skeletal myocytes.

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Silencing miR-106b improves palmitic acid-induced mitochondrial dysfunction and insulin resistance in skeletal myocytes.

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Silencing miR-106b improves palmitic acid-induced mitochondrial dysfunction and insulin resistance in skeletal myocytes.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Gao, Yuan-Fu Zhao, Ya-Ping Gao, Chun-Lin Cai, Xiao-Yi Fan, Zhong-Min Zhang, Ying Liu, Meng-Yuan Xia, Zheng-Kun
Description	Author Affiliation: Zhang Y ( Department of Pediatrics, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, Jiangsu 210002, P.R. China.); Zhao YP ( Department of Pediatrics, The 82nd Hospital of the People's Liberation Army, Huai'an, Jiangsu 223001, P.R. China.); Gao YF ( Department of Pediatrics, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, Jiangsu 210002, P.R. China.); Fan ZM ( Department of Pediatrics, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, Jiangsu 210002, P.R. China.); Liu MY ( Department of Pediatrics, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, Jiangsu 210002, P.R. China.); Cai XY ( Department of Pediatrics, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, Jiangsu 210002, P.R. China.); Xia ZK ( Department of Pediatrics, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, Jiangsu 210002, P.R. China.); Gao CL ( Department of Pediatrics, Jinling Hospital, Nanjing University, School of Medicine, Nanjing, Jiangsu 210002, P.R. China.)
Abstract	MicroRNA106b (miR106b) is reported to correlate closely with skeletal muscle insulin resistance. In the current study the effect of miR106b on palmitic acid (PA)induced mitochondrial dysfunction and insulin resistance was investigated in C2C12 myotubes via the silencing of miR106b. MiR106b expression was increased under PA treatment, while miR106b loss of function improved insulin sensitivity by upregulating its target mitofusin2 (Mfn2) in C2C12 myocytes. Furthermore, miR106b loss of function partly improved mitochondrial morphological lesions and increased the levels of mitochondial DNA and intracellular adenosine triphosphate that had been impaired by PA exposure in C2C12 myocytes. MiR106b loss of function attenuated the levels of intracellular reactive oxygen species (ROS), and upregulated the expression levels of the estrogenrelated receptor (ERR) /peroxisome proliferative activated receptor Î³ coactivator (PGC)1 /Mfn2 axis under PA exposure. In addition, miR106b negatively regulated skeletal muscle mitochondrial function and insulin sensitivity under PAinduced insulin resistance by targeting Mfn2, which may be associated with reduced ROS and upregulation of the ERR /PGC1 /Mfn2 axis.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	5
Volume Number	11
Language	English
Publisher	Spandidos Publications
Publisher Date	2015-05-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Gene Silencing Insulin Resistance Genetics Micrornas Mitochondria Drug Effects Metabolism Muscle Fibers, Skeletal Palmitic Acid Pharmacology Adenosine Triphosphate Animals Cell Line Gene Expression Regulation Mice Reactive Oxygen Species Receptors, Estrogen Transcription Factors Research Support, Non-u.s. Gov't Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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