摘要
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.
出处
《中华内分泌代谢杂志》
CAS
CSCD
北大核心
2007年第1期5-7,共3页
Chinese Journal of Endocrinology and Metabolism