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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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Gradual deterioration of pancreatic beta cells is a conundrum still to be resolved in the diabetes field. The toxicity manifested by high level of glucose and saturated fatty acid (SFA), which is collectively termed as glucolipotoxicity, has been accepted as a predominant factor of beta cell dysfunction or failure. In this study, we examined the effect of TRIP (Triazolo[3,4-a]phthalazine)-16, a compound derivatized from TRIP which had been identified in a high throughput screening to discover chemicals protecting INS-1 cells from glucolipotoxicity. We also investigated its mode of action to reduce glucolipotoxicity, especially regarding modulation of lipid metabolism. From a series of cell-based experiments, we observed that TRIP-16 reduced fatty acid-induced triglyceride (TG) accumulation, whereas it increased oxidation rate of glucose or palmitate. The compound also reduced reactive oxygen species generated by palmitate and upregulated expression levels of carnitine palmitoyltransferase-1a (CPT-1a), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-$1{\alpha}$) and uncoupling protein 2 (UCP-2), implicating that it can facilitate mitochondrial energy metabolism to oxidize palmitate. In terms of beta cell functioning, TRIP-16 augmented glucose-stimulated insulin secretion (GSIS) per se. Taken together, our data strongly suggest that TRIP-16 can be a potential drug candidate for prevention of type 2 diabetes through beta cell protection.
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참고문헌 (28)
참고문헌 신청
Prentki, M / 2006 / Islet beta cell failure in type 2diabetes / J. Clin. Invest 116:1802
Montane, J / 2014 / Stress and the inflammatory process: a major cause of pancreatic cell death in type 2 diabetes / Diabetes Metab. Syndr. Obes 7:25
Robertson, R. P / 2003 / Glucose toxicity in beta-cells: type 2 diabetes, good radicals gone bad, and the glutathione connection / Diabetes 52:581
Park, J. H / 2014 / Melatonin prevents pancreatic beta-cell loss due to glucotoxicity: the relationship between oxidative stress and endoplasmic reticulum stress / J. Pineal. Res 56:143
Tanaka, Y / 1999 / Prevention of glucose toxicity in HIT-T15cells and Zucker diabetic fatty rats by antioxidants / Proc. Natl. Acad. Sci. U. S. A 96:10857
Montane, J / 2014 / Stress and the inflammatory process: a major cause of pancreatic cell death in type 2 diabetes / Diabetes Metab. Syndr. Obes 7:25
Robertson, R. P / 2003 / Glucose toxicity in beta-cells: type 2 diabetes, good radicals gone bad, and the glutathione connection / Diabetes 52:581
Park, J. H / 2014 / Melatonin prevents pancreatic beta-cell loss due to glucotoxicity: the relationship between oxidative stress and endoplasmic reticulum stress / J. Pineal. Res 56:143
Tanaka, Y / 1999 / Prevention of glucose toxicity in HIT-T15cells and Zucker diabetic fatty rats by antioxidants / Proc. Natl. Acad. Sci. U. S. A 96:10857
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