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. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Project 2. 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 attenuates the development of obesity in mice fed a high fat diet. Our preliminary studies also demonstrate that the reduction in body weight and adipose tissue mass in the mice is not due reductions in food consumption or physical activity. Our data suggests that there is a reduction in energy expenditure in the mice which suggests that the reduction in body weight gain and adipose tissue mass may be due to an increase in fat cell break down. The future direction on our project will determine if the mice have an increase in fat cell break down and determine if reductions in PGE2 is responsible for the reduction in fat cell break down and how this occurs. During the development of obesity, inflammatory cells move into the fat tissue. Our studies will also determine if reductions in PGE2 from inflammatory cells or fat cells is responsible for the reduction in weight gain.