Deficiency of MGAT2 increases energy expenditure without high-fat feeding and protects genetically obese mice from excessive weight gain

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A Recurring Problem With the Analysis of Energy Expenditure in Genetic Models Expressing Lean and Obese Phenotypes

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Intestine-specific expression of acyl CoA:diacylglycerol acyltransferase 1 reverses resistance to diet-induced hepatic steatosis and obesity inDgat1−/−mice

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Bowels control brain: gut hormones and obesity

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Role of MGAT2 and DGAT1 in the release of gut peptides after triglyceride ingestion

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Triacylglycerol synthesis and energy metabolism: a gut reaction?

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Deficiency of the intestinal enzyme acyl CoA:monoacylglycerol acyltransferase-2 protects mice from metabolic disorders induced by high-fat feeding

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