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High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds
Published on: January 23, 2018
Far-infrared radiation prevents decline in β-cell mass and function in diabetic mice via the mitochondria-mediated
Yung-Ho Hsu1, Yen-Cheng Chen2, Yu-Wei Chen3
1Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taiwan; Division of Nephrology, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, Taiwan.
Abstract:
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.
Insights
Far-infrared (FIR) radiation preserves pancreatic beta-cell function and survival in type 2 diabetes. FIR enhances insulin secretion by upregulating promyelocytic leukemia zinc finger protein (PLZF) and mitochondrial function via the Sirtuin1 (Sirt1) pathway.
Area of Science:
- Endocrinology and Metabolism
- Cell Biology
- Biomedical Engineering
Background:
- Type 2 diabetes mellitus (DM) is characterized by declining pancreatic beta-cell mass and function.
- Beta-cell preservation is a key therapeutic target for type 2 DM.
- Far-infrared (FIR) radiation has shown protective effects on vascular endothelium in diabetic models.
Purpose of the Study:
- To investigate the effects of FIR (8-10 μm) on beta-cell survival and insulin secretion in type 2 DM.
- To elucidate the molecular mechanisms underlying FIR's action on beta-cells.
Main Methods:
- Utilized nicotinamide-streptozotocin-induced type 2 DM mouse models.
- Administered FIR (8-10 μm) and assessed pancreatic islet integrity and insulin secretion.
- Investigated the roles of promyelocytic leukemia zinc finger protein (PLZF) and Sirtuin1 (Sirt1) using cell lines and specific inhibitors/siRNA.
- Analyzed mitochondrial function and NAD+/NADH ratios.
Main Results:
- FIR reduced pancreatic islet loss and increased insulin secretion in DM mice.
- FIR upregulated PLZF, conferring anti-apoptotic effects on beta-cells.
- FIR enhanced mitochondrial function, NAD+/NADH ratio, and Sirtuin1 (Sirt1) expression.
- Inhibition of mitochondrial complex I, Sirt1, or PLZF blocked FIR's beneficial effects on insulin secretion and beta-cell survival.
Conclusions:
- FIR radiation effectively preserves beta-cell mass and function in type 2 DM.
- FIR-mediated protection involves enhanced mitochondrial function, PLZF activation, and Sirtuin1 (Sirt1) pathway.
- FIR represents a potential therapeutic strategy for managing type 2 diabetes by protecting beta-cells.
