Humanin promotes mitochondrial biogenesis in pancreatic MIN6 β-cells

Biochem Biophys Res Commun. 2018 Feb 26;497(1):292-297. doi: 10.1016/j.bbrc.2018.02.071.

Qingqing Qin ¹, Jieqiong Jin ², Fang He ¹, Yongqin Zheng ³, Tingting Li ¹, Yun Zhang ¹, Jundong He ⁴

Affiliations

1 Medical Faculty, Kunming University of Science and Technology, Kunming 650500, China; Institute of Basic and Clinical Medicine, Key Laboratory for Clinical Virology, Key Laboratory for Birth Defects and Genetic Diseases, The First People's Hospital of Yunnan Province, Kunming 650032, China; The Affiliated Hospital of Kunming University of Science and Technology, Kunming 650032, China.
2 State Key Laboratory of Genetic Resources and Evolution, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, China.
3 Institute of Basic and Clinical Medicine, Key Laboratory for Clinical Virology, Key Laboratory for Birth Defects and Genetic Diseases, The First People's Hospital of Yunnan Province, Kunming 650032, China; The Affiliated Hospital of Kunming University of Science and Technology, Kunming 650032, China.
4 Institute of Basic and Clinical Medicine, Key Laboratory for Clinical Virology, Key Laboratory for Birth Defects and Genetic Diseases, The First People's Hospital of Yunnan Province, Kunming 650032, China; The Affiliated Hospital of Kunming University of Science and Technology, Kunming 650032, China; Medical Faculty, Kunming University of Science and Technology, Kunming 650500, China. Electronic address: [email protected].

PMID: 29432738 DOI: 10.1016/j.bbrc.2018.02.071

Abstract

Mitochondrial dysfunction is associated with β-cell failure and Insulin resistance in diabetes. Humanin is an endogenous cytoprotective peptide. In the current study, we aimed to define the effects of Humanin on mitochondrial biogenesis in pancreatic β-cells. Our findings demonstrated that Humanin treatment significantly increased the expression of PGC-1α and its downstream target genes NRF1 and TFAM in MIN6 β-cells. Notably, Humanin treatment significantly promoted mitochondrial biogenesis by increasing mitochondrial mass, elevating mtDNA/nDNA ratio, and stimulating the expression of cytochrome B, which were suppressed by the specific AMPK Inhibitor compound C. Indeed, Humanin treatment caused the phosphorylation of AMPK, which was involved in the induction of PGC-1α, NRF1, and TFAM by Humanin. Importantly, our findings indicate that Humanin treatment led to a possible functional gain of the mitochondria by increasing ATP levels and respiratory rate. Our findings provided a new insight into the molecular mechanisms of action by which Humanin improves pancreatic β-cell function via enhanced mitochondrial mass and performance.

Keywords

Diabetes; Humanin; Mitochondria biogenesis; PGC-1α; mtDNA.

Name
Email *

	Sorry, but the email address you supplied was invalid.