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Diglyceride acyltransferase (DGAT) is a membrane-bound enzyme that catalyzes the final and only committed step in the biosynthesis of triglycerides from diacylglycerol and fatty acyl-CoA. This reaction is essential for energy storage as fat, intestinal absorption of dietary fats, adipose tissue formation, milk production, and overall lipid homeostasis. There are two main isoforms in mammals—DGAT1 and DGAT2—which perform similar biochemical functions but have distinct tissue distributions and regulatory properties. Disruption or pharmacological inhibition of these enzymes affects body fat accumulation, energy balance, lactation ability, skin integrity, and may influence susceptibility to obesity-related diseases. Because of its central role in triglyceride metabolism—and its impact on conditions like obesity—DGAT is considered a promising therapeutic target for metabolic disorders[1][2][4][5].
Inhibition of DGAT reduces triglyceride synthesis and fat absorption/storage (primarily via blocking the final step in triacylglycerol biosynthesis)
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