2. Academic Validation
  3. Irisin reverses insulin resistance in C2C12 cells via the p38-MAPK-PGC-1α pathway

Irisin reverses insulin resistance in C2C12 cells via the p38-MAPK-PGC-1α pathway

  • Peptides. 2019 Sep;119:170120. doi: 10.1016/j.peptides.2019.170120.
Xiao Ye 1,  YiMin Shen 2,  Chao Ni 3,  Jun Ye 4,  Yubo Xin 1,  Wei Zhang 5,  YueZhong Ren 6
Affiliations

Affiliations

  • 1 Department of Endocrinology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou 310003, China.
  • 2 Department of Endocrinology, Second Affiliated Hospital, Medical School of Zhejiang University, Hangzhou 310003, China.
  • 3 Key Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou 310003, China.
  • 4 Department of Gastroenterology, Second Affiliated Hospital, Medical School of Zhejiang University, Hangzhou 310003, China.
  • 5 Department of Endocrinology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou 310003, China; Key Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou 310003, China. Electronic address: [email protected].
  • 6 Department of Endocrinology, Second Affiliated Hospital, Medical School of Zhejiang University, Hangzhou 310003, China. Electronic address: [email protected].
PMID: 31351089 DOI: 10.1016/j.peptides.2019.170120
Abstract

Insulin resistance (IR) is a fundamental pathogenic factor shared by a myriad of metabolic disorders, including obesity and type 2 diabetes. The mechanism of IR is usually accompanied by mitochondrial dysfunction. Irisin has been proposed to act as a hormone in the regulation of energy homeostasis and metabolism. However, the effects of irisin on IR and mitochondrial function have not yet been fully investigated. Here, our research shows that irisin increases glucose uptake in C2C12 myoblast cells via the p38-mitogen-activated protein kinase (MAPK)-PGC-1α pathway. Irisin can also enhance mitochondrial function and mitochondrial respiration. Moreover, irisin stimulates Autophagy via PGC-1α. Collectively, these data provide basic evidence to support the therapeutic potential of irisin for IR, which may rely on p38-MAPK-PGC-1α pathway activation and enhance mitochondrial function.

Keywords

Insulin resistance; Irisin; PGC-1 α; p38.

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