Division of Metabolic and Vascular Health, Warwick Medical School, University of Warwick, Coventry KA4 7AL, UK.
Biochem J. 2013 Apr 1;451(1):1-12. doi: 10.1042/BJ20121689.
lThe liver regulates both glycaemia and triglyceridaemia. Hyperglycaemia and hypertriglyceridaemia are both characteristic of (pre)diabetes. Recent observations on the specialised role of DGAT2 (diacylglycerol acyltransferase 2) in catalysing the de novo synthesis of triacylglycerols from newly synthesized fatty acids and nascent diacylglycerols identifies this enzyme as the link between the two. This places DGAT2 at the centre of carbohydrate-induced hypertriglyceridaemia and hepatic steatosis. This function is complemented, but not substituted for, by the ability of DGAT1 to rescue partial glycerides from complete hydrolysis. In peripheral tissues not normally considered to be lipogenic, synthesis of triacylglycerols may largely bypass DGAT2 except in hyperglycaemic/hyperinsulinaemic conditions, when induction of de novo fatty acid synthesis in these tissues may contribute towards increased triacylglycerol secretion (intestine) or insulin resistance (adipose tissue, and cardiac and skeletal muscle).
肝脏调节血糖和甘油三酯水平。高血糖和高甘油三酯血症都是（前）糖尿病的特征。最近观察到 DGAT2（二酰基甘油酰基转移酶 2）在催化新合成的脂肪酸和新生二酰基甘油从头合成三酰甘油方面的特殊作用，将这种酶确定为两者之间的联系。这使 DGAT2 处于碳水化合物诱导的高甘油三酯血症和肝脂肪变性的中心位置。这种功能得到了 DGAT1 的补充，但不能替代，DGAT1 能够将部分甘油从完全水解中挽救出来。在通常不被认为是生脂的外周组织中，三酰甘油的合成可能主要绕过 DGAT2，除非在高血糖/高胰岛素血症的情况下，此时这些组织中从头合成脂肪酸的诱导可能导致三酰甘油分泌增加（肠道）或胰岛素抵抗（脂肪组织以及心脏和骨骼肌）。
