DGAT and triglyceride synthesis: a new target for obesity treatment?
Because triglycerides are considered essential for survival and their synthesis has been thought to occur through a single mechanism, inhibiting triglyceride synthesis has been largely unexplored as a possible target for obesity treatment. However, recent studies indicate that mice lacking acyl CoA:diacylglycerol acyltransferase (DGAT), a key enzyme in triglyceride synthesis, are viable and resistant to diet-induced obesity. Unexpectedly, this resistance is caused by a mechanism involving increased energy expenditure. These findings suggest that inhibiting specific components of triglyceride synthesis, such as DGAT, is feasible and may represent a novel approach to treating obesity.
Chen
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HC
Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, CA 94141-9100, USA. hcc1@itsa.ucsf.edu
Farese
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RV
D000217:Acyltransferases / Q000378:metabolism*; D000818:Animals; D051048:Diacylglycerol O-Acyltransferase; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism; D051379:Mice; D009765:Obesity / Q000378:metabolism / Q000628:therapy*; D014280:Triglycerides / Q000096:biosynthesis* / Q000378:metabolism*
D014280:Triglycerides; D000217:Acyltransferases; C494882:Dgat1 protein, mouse; D051048:Diacylglycerol O-Acyltransferase; D005947:Glucose