The EP3 receptor – one of the receptors for the prostaglandin PGE2 – has an important role in adipose (fat) tissue physiology, Vanderbilt investigators reported recently in the journal Endocrinology.
PGE2 and other prostaglandins are mediators of inflammation and may contribute to obesity-related insulin resistance and type 2 diabetes. Richard Breyer, Ph.D., and colleagues explored metabolic responses in mice missing the EP3 receptor.
They found that when these mice were fed a high-fat diet, they gained more weight compared to mice with the EP3 receptor. They also had increased epididymal fat mass (an abdominal fat storage area in male mice) and fat cell size, and a redistribution of lipids from fat to other tissues, including liver and skeletal muscle. Mice missing the EP3 receptor and eating a high-fat diet became insulin resistant and had elevated blood glucose.
The findings demonstrate the effects of disrupted PGE2-EP3 signaling on diabetes in a setting of diet-induced obesity and add to the mounting role for inflammatory mediators in obesity.
This research was supported by grants from the National Institutes of Health (DK046205, DK037097, DK072473, DK089572, DK104211, DK097829) and the Juvenile Diabetes Research Foundation, and by Merit Awards from the Department of Veterans Affairs.
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