安普克
胰岛素抵抗
蛋白激酶A
代谢综合征
糖尿病
脂质代谢
AMP活化蛋白激酶
医学
内分泌学
生物信息学
疾病
生物
内科学
激酶
细胞生物学
作者
Neil B. Ruderman,Marc Prentki
摘要
Patients with the metabolic syndrome are characterized by insulin resistance, obesity and a predisposition to hypertension, dyslipidaemia, pancreatic β-cell dysfunction, type 2 diabetes and premature atherosclerosis. Here we review the hypothesis that a common feature linking these multiple abnormalities is dysregulation of the AMP-activated protein kinase (AMPK)/malonyl-CoA fuel-sensing and signalling network. It is proposed that such dysregulation leads to alterations in cellular fatty-acid metabolism that in turn cause ectopic lipid accumulation, cellular dysfunction and ultimately disease. Evidence is also presented that factors that activate AMP kinase and/or reduce malonyl-CoA levels might reverse these abnormalities or prevent them from occurring.
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