期刊
BIOCHEMICAL JOURNAL
卷 451, 期 -, 页码 1-12出版社
PORTLAND PRESS LTD
DOI: 10.1042/BJ20121689
关键词
de novo fatty acid synthesis; diacylglycerol acyltransferase; heart; hypertriglyceridaemia; intestine; lipogenesis; liver; muscle
资金
- Medical Research Council (UK)
- Diabetes UK
- British Heart Foundation
- Biotechnology and Biological Sciences Research Council (UK)
The 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 triacylgycerols 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).
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