Qin 2018 Biochem Biophys Res Commun

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Qin Q, Jin J, He F, Zheng Y, Li T, Zhang Y, He J (2018) Humanin promotes mitochondrial biogenesis in pancreatic MIN6 β-cells. Biochem Biophys Res Commun 497:292-7.

» PMID: 29432738

Qin Q, Jin J, He F, Zheng Y, Li T, Zhang Y, He J (2018) Biochem Biophys Res Commun

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 Bioblast editor: Kandolf G O2k-Network Lab: CN Tianjin Zhang Y


Labels: MiParea: Respiration, mt-Biogenesis;mt-density, mt-Membrane, mtDNA;mt-genetics 


Organism: Mouse  Tissue;cell: Islet cell;pancreas;thymus, Other cell lines 



HRR: Oxygraph-2k 

Labels, 2018-03