MICROSOMAL PROSTAGLANDIN E SYNTHASE-1 DEFICIENCY ATTENUATES DIET-INDUCED OBESITY

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Project 2 Description: Microsomal prostaglandin E synthase-1 deficiency attenuates the development of development of diet-induced obesity in male mice The focus of our project is to determine the effect of inflammatory molecules on the development and/or progression of diet-induced obesity. Previous studies have suggested that prostaglandin E2 (PGE2), which is an inflammatory mediator that is produced at a very high concentration during inflammation, can inhibit break down of fat cells to free fatty acids and glycerol, which may result in a decrease in fat mass. Preliminary data from our studies demonstrate that deficiency of the major enzyme, microsomal prostaglandin E synthase-1, which produces PGE2 during an inflammatory response attenuates the development of obesity in mice fed a high fat diet. Our data also demonstrate that the reduction in body weight and adipose tissue mass in the mice is not due to reductions in food consumption or physical activity but due to an increase in energy expenditure in the mice.