脂毒性及其防治的一个关键靶点——AMPK

Lipotoxicity and AMPK-- a key target for its prevention and treatment

当过多摄入的能量超出了脂肪组织的贮存容量时，脂质溢出进入胰腺、肝脏及骨骼肌等非脂肪组织贮存，诱发胰岛素抵抗，损伤胰岛β细胞功能，导致2型糖尿病及其并发症的发生。运动，饮食控制及激活“代谢总开关”一磷酸腺苷活化蛋白激酶（AMPK）的药物，二甲双胍、罗格列酮可促进外周组织的脂质氧化，降低脂质的异位堆积，阻止或延缓2型糖尿病的发生。因此，AMPK可能成为防治脂毒性的关键靶点。

When excessive energy intake overrides the storage capacity of adipose tissue, lipid spills and deposits in non-fat tissues such as pancreatic β-cell, liver, skeletal muscle, which leads to insulin resistance, islets β-cell dysfunction and overt type 2 diabetes and its complications. As exercise, diet, mefformin and rosiglitazone that activate the ＂metabolic master switch＂ AMP-activated protein kinase （AMPK）, increase lipid oxidation and decrease the ectopic accumulation of lipid, which prevent or delay the onset of type 2 diabetes. Therefore, AMPK seems to be a key target for preventing lipotoxicity.