Far-infrared radiation prevents decline in β-cell mass and function in diabetic mice via the mitochondria-mediated Sirtuin1 pathway

研究成果: 雜誌貢獻文章


Insulin deficiency in type 2 diabetes mellitus (DM) involves a decline in both pancreatic β-cell mass and function. Enhancing β-cell preservation represents an important therapeutic strategy to treat type 2 DM. Far-infrared (FIR) radiation has been found to induce promyelocytic leukemia zinc finger protein (PLZF) activation to protect the vascular endothelium in diabetic mice. The influence of FIR on β-cell preservation is unknown. Our previous study reveals that the biologically effective wavelength of FIR is 8–10 μm. In the present study, we investigated the biological effects of FIR (8–10 μm) on both survival and insulin secretion function of β-cells. FIR reduced pancreatic islets loss and increased insulin secretion in nicotinamide-streptozotocin-induced DM mice, but only promoted insulin secretion in DM PLZF− / − mice. FIR-upregulated PLZF to induce an anti-apoptotic effect in a β cell line RIN-m5f. FIR also upregulated mitochondrial function and the ratio of NAD+/NADH, and then induced Sirtuin1 (Sirt1) expression. The mitochondria Complex I inhibitor rotenone blocked FIR-induced PLZF and Sirt1. The Sirt1 inhibitor EX527 and Sirt1 siRNA inhibited FIR-induced PLZF and insulin respectively. Sirt1 upregulation also increased CaV1.2 expression and calcium influx that promotes insulin secretion in β-cells. In summary, FIR-enhanced mitochondrial function prevents β-cell apoptosis and enhances insulin secretion in DM mice through the Sirt1 pathway.
期刊Metabolism: Clinical and Experimental
出版狀態已發佈 - 三月 2020


ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism