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

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 项目2：微粒体前列腺素E合成酶-1缺乏延缓饮食诱导的雄性小鼠肥胖的发展 我们项目的重点是确定炎症分子在饮食诱导肥胖的发展和/或进展中的作用。以前的研究表明，前列腺素E2(PGE2)是一种炎症介质，在炎症过程中产生很高的浓度，可以抑制脂肪细胞分解为游离脂肪酸和甘油，这可能导致脂肪质量的减少。我们研究的初步数据表明，产生PGE2的主要酶--微粒体前列腺素E合成酶-1的缺乏可以减缓喂食高脂饮食的小鼠肥胖的发展。我们的初步研究还表明，小鼠体重和脂肪组织质量的减少并不是食物消耗或体力活动的适当减少。我们的数据表明，小鼠的能量消耗减少，这表明体重增加和脂肪组织质量的减少可能是由于脂肪细胞分解的增加。我们项目的未来方向将确定小鼠的脂肪细胞分解是否增加，并确定PGE2的减少是否导致脂肪细胞分解的减少以及这是如何发生的。在肥胖的发展过程中，炎症细胞进入脂肪组织。我们的研究还将确定炎性细胞或脂肪细胞中PGE2的减少是否与体重增加的减少有关。

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.