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甘油三酯(TG)是真核细胞中最重要的能量储存形式,尽管它是正常生理所必需,但过量堆积,就会导致肥胖。因此抑制TG的合成可能改善肥胖以及与之相关的症状。脂酰辅酶A:二酰基甘油酰转移酶(DGAT)是以甘油二酯和脂酰辅酶A为底物,催化甘油三酯合成途径的最后一步反应的关键酶。DGAT1基因敲除(Dgat1-/-)小鼠对肥胖有抵抗力,并且增加了对胰岛素和瘦素的敏感性,这种小鼠对饮食诱导的脂肪肝也有抵抗力。此外,DGAT1的缺乏影响脂肪源性因子的表达和分泌,从而调节能量和葡萄糖的代谢。这些研究提示DGAT1有望成为治疗肥胖和2-型糖尿病的新靶点。
Triglyceride (TG) is the most important form of energy storage in eukaryotic cells. Although it is necessary for normal physiology, excessive accumulation can lead to obesity. Therefore, inhibition of TG synthesis may improve obesity and its associated symptoms. Acyl-CoA: Diacylglycerol acyltransferase (DGAT) is a key enzyme that catalyzes the final reaction of triglyceride synthesis with diglyceride and acyl-CoA as substrates. DGAT1 knockout (Dgat1 - / -) mice are obese and increase their sensitivity to insulin and leptin, which are also resistant to diet-induced fatty liver. In addition, the lack of DGAT1 affects the expression and secretion of adipose-derived factors, thereby regulating energy and glucose metabolism. These studies suggest that DGAT1 is expected to become a new target for the treatment of obesity and type 2 diabetes.