Protein Receptor Controls Fat Storage

Researchers working with a mouse model for obesity have found that when activated, the protein receptor peroxisome proliferators-activated receptor (PPARd) depleted fat deposits in the mice but that when mice lacked activated PPARd, they tended toward obesity.

Investigators from the Salk Institute (La Jolla, CA, USA) compared mice that had been genetically engineered to express activated PPARd with a group of normal animals. They found that mice with an activated PPARd gene weighed about 20% less than normal mice, even though both groups received the same food at the same rate. When the mice had reached a year of age, the difference in weight of the PPARd group widened, to 35% less than for the normal mice. The presence of activated PPARd also prevented mice from becoming obese when fed a high calorie diet. These findings were published in the April 18, 2003, issue of Cell.

"We have long known that excess calories are warehoused in fat tissue for future use,” explained senior author Professor Ronald M. Evans, chairman of the developmental and molecular biology department of the Salk Institute. "We also know that fat is released and consumed in times when energy is needed, such as from exercise or shivering from cold exposure. This study shows us that PPARd is an important regulator of this function. By exploiting PPARd, we hope to design drugs that can control how much fat is stored in the body.”




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The Salk Institute