کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1932549 1050584 2010 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Activation of PPARδ up-regulates fatty acid oxidation and energy uncoupling genes of mitochondria and reduces palmitate-induced apoptosis in pancreatic β-cells
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Activation of PPARδ up-regulates fatty acid oxidation and energy uncoupling genes of mitochondria and reduces palmitate-induced apoptosis in pancreatic β-cells
چکیده انگلیسی

Recent evidence indicates that decreased oxidative capacity, lipotoxicity, and mitochondrial aberrations contribute to the development of insulin resistance and type 2 diabetes. The goal of this study was to investigate the effects of peroxisome proliferator-activated receptor δ (PPARδ) activation on lipid oxidation, mitochondrial function, and insulin secretion in pancreatic β-cells. After HIT-T15 cells (a β-cell line) were exposed to high concentrations of palmitate and GW501516 (GW; a selective agonist of PPARδ), we found that administration of GW increased the expression of PPARδ mRNA. GW-induced activation of PPARδ up-regulated carnitine palmitoyltransferase 1 (CPT1), long-chain acyl-CoA dehydrogenase (LCAD), pyruvate dehydrogenase kinase 4 (PDK4), and uncoupling protein 2 (UCP2); alleviated mitochondrial swelling; attenuated apoptosis; and reduced basal insulin secretion induced by increased palmitate in HIT cells. These results suggest that activation of PPARδ plays an important role in protecting pancreatic β-cells against aberrations caused by lipotoxicity in metabolic syndrome and diabetes.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 391, Issue 3, 15 January 2010, Pages 1567–1572
نویسندگان
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