کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1936764 | 1050702 | 2008 | 7 صفحه PDF | دانلود رایگان |

It is well known that the activation of AMP-activated protein kinase (AMPK) represses insulin gene expression and glucose-stimulated insulin secretion. However, how this effect is achieved and the effects of AMPK activation on glucolipotoxicity-induced β-cell dysfunction have not been elucidated. We investigate whether BETA2 gene expression are involved in the AMPK-mediated regulation of insulin gene expression in normal and dysfunctional β-cells. BETA2 gene expression and protein levels were significantly decreased by AICAR treatment and those were associated with the suppression of BETA2 promoter activity and DNA binding activity. These results demonstrate that the expressions of BETA2 and insulin gene are positively regulated by glucose and negatively by AMPK. Therefore, AMPK may function as a key molecule, which conveys extracellular metabolic signals into the cells and finely tunes expression of β-cell specific transcription factors in response to glucose level.
Journal: Biochemical and Biophysical Research Communications - Volume 365, Issue 4, 25 January 2008, Pages 614–620