A molecular switch known to regulate fat metabolism appears to prevent obesity in laboratory mice. The discovery of the switch could lead to treatments for obesity and disorders associated with it, such as heart disease and type 2 diabetes.
The Salk Institute for Biological Studies study, led by professor Ronald Evans and his postdoctoral fellow Yong-Xu Wang, appears in the September issue of the Public Library of Science Biology journal (PLoS Biology).
The team discovered that activation of the switch, a receptor called PPAR-delta, increases the rate at which the body burns fat. This makes PPAR-delta an exciting potential target for drugs that treat diabetes and lipid disorders.
By turning on PPAR-delta, the team produced highly efficient muscle fibers that burned fat more rapidly. As a result, the mice were almost unable to gain weight even in the absence of exercise.
Evans and his team treated normal mice with an experimental drug called GW501516 that activates PPAR-delta. These mice also expressed genes for slow-twitch muscles and gained less weight when given a high-fat diet.
This drug is in the earliest stages of being tested on people for its effects on obesity and other disorders of fat metabolism such as high blood cholesterol.