NDLI: Adult-onset deficiency of acyl CoA:monoacylglycerol acyltransferase 2 protects mice from diet-induced obesity and glucose intolerance.

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Adult-onset deficiency of acyl CoA:monoacylglycerol acyltransferase 2 protects mice from diet-induced obesity and glucose intolerance.

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Adult-onset deficiency of acyl CoA:monoacylglycerol acyltransferase 2 protects mice from diet-induced obesity and glucose intolerance.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Banh, Taylor Nelson, David W. Gao, Yu Huang, Ting-Ni Yen, Mei-I Yen, Chi-Liang E.
Description	Author Affiliation: Banh T ( Department of Nutritional Sciences, University of Wisconsin-Madison, WI 53706.); Nelson DW ( Department of Nutritional Sciences, University of Wisconsin-Madison, WI 53706.); Gao Y ( Department of Nutritional Sciences, University of Wisconsin-Madison, WI 53706.); Huang TN ( Department of Nutritional Sciences, University of Wisconsin-Madison, WI 53706.); Yen MI ( Department of Nutritional Sciences, University of Wisconsin-Madison, WI 53706.); Yen CL ( Department of Nutritional Sciences, University of Wisconsin-Madison, WI 53706.)
Abstract	Acyl-CoA:monoacylglycerol acyltransferase (MGAT) 2 catalyzes triacylglycerol (TAG) synthesis, required in intestinal fat absorption. We previously demonstrated that mice without a functional MGAT2-coding gene (Mogat2(-/-)) exhibit increased energy expenditure and resistance to obesity induced by excess calories. One critical question raised is whether lacking MGAT2 during early development is required for the metabolic phenotypes in adult mice. In this study, we found that Mogat2(-/-) pups grew slower than wild-type littermates during the suckling period. To determine whether inactivating MGAT2 in adult mice is sufficient to confer resistance to diet-induced obesity, we generated mice with an inducible Mogat2-inactivating mutation. Mice with adult-onset MGAT2 deficiency (Mogat2(AKO)) exhibited a transient decrease in food intake like Mogat2(-/-) mice when fed a high-fat diet and a moderate increase in energy expenditure after acclimatization. They gained less weight than littermate controls, but the difference was smaller than that between wild-type and Mogat2(-/-) mice. The moderate reduction in weight gain was associated with reduced hepatic TAG and improved glucose tolerance. Similar protective effects were also observed in mice that had gained weight on a high-fat diet before inactivating MGAT2. These findings suggest that adult-onset MGAT2 deficiency mitigates metabolic disorders induced by high-fat feeding and that MGAT2 modulates early postnatal nutrition and may program metabolism later in life.
File Format	HTM / HTML
ISSN	00222275
e-ISSN	15397262
DOI	10.1194/jlr.M055228
Journal	The Journal of Lipid Research
Issue Number	2
Volume Number	56
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	2015-02-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Biochemistry Acyltransferases Metabolism Dietary Fats Adverse Effects Glucose Intolerance Enzymology Prevention & Control Obesity Genetics Animals Physiology Energy Metabolism Mice
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Endocrinology

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Adult-onset deficiency of acyl CoA:monoacylglycerol acyltransferase 2 protects mice from diet-induced obesity and glucose intolerance[S]

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Adult-onset deficiency of acyl CoA:monoacylglycerol acyltransferase 2 protects mice from diet-induced obesity and glucose intolerance.

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Adult-onset deficiency of acyl CoA:monoacylglycerol acyltransferase 2 protects mice from diet-induced obesity and glucose intolerance.