کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1984684 | 1539986 | 2006 | 12 صفحه PDF | دانلود رایگان |

Type 2 diabetes is the most prevalent and serious metabolic disease affecting people all over the world. Pancreatic β-cell dysfunction and insulin resistance are the hallmark of type 2 diabetes. Normal β-cells can compensate for insulin resistance by increasing insulin secretion and/or β-cell mass, but insufficient compensation leads to the onset of glucose intolerance. Once hyperglycemia becomes apparent, β-cell function gradually deteriorates and insulin resistance aggravates. Under diabetic conditions, oxidative stress and endoplasmic reticulum stress are induced in various tissues, leading to activation of the c-Jun N-terminal kinase pathway. The activation of c-Jun N-terminal kinase suppresses insulin biosynthesis and interferes with insulin action. Indeed, suppression of c-Jun N-terminal kinase in diabetic mice improves insulin resistance and ameliorates glucose tolerance. Thus, the c-Jun N-terminal kinase pathway plays a central role in pathogenesis of type 2 diabetes and could be a potential target for diabetes therapy.
Journal: The International Journal of Biochemistry & Cell Biology - Volume 38, Issues 5–6, May–June 2006, Pages 782–793