ATM Regulates Adipocyte Differentiation and Contributes to Glucose Homeostasis

摘要: Summary Ataxia-telangiectasia (A-T) patients occasionally develop diabetes mellitus. However, only limited attempts have been made to gain insight into the molecular mechanism of mellitus development in A-T patients. We found that Atm −/− mice were insulin resistant and possessed less subcutaneous adipose tissue as well a lower level serum adiponectin than +/+ mice. Furthermore, in vitro studies revealed impaired adipocyte differentiation cells caused by lack induction C/EBPα PPARγ, crucial transcription factors involved differentiation. Interestingly, ATM was activated stimuli induced differentiation, binding C/EBPβ p300 transcriptional regulation Thus, our study sheds light on poorly understood role pathogenesis glucose intolerance provides insight metabolism.