Control mice were fed standard chow with 4. Get the latest science news with sciencedaily’s free email newsletters, updated daily and weekly. Tell us what you think of sciencedaily — we welcome both positive and negative comments. Obesity is associated with a state of chronic, low-grade inflammation that leads to insulin resistance, which is usually the first step in the development of type 2 diabetes. When the high-fat diet is fed to a normal mouse, ikke protein-kinase levels rise, the metabolic rate slows, and the animal gains weight. 5 percent of its calories from fat. When the switch is turned off, even high-fat-diet mice remain thin.
Fat mice lick prevent gene. All animal use was conducted in compliance with the institute of laboratory animal research’s guide for the care and use of laboratory animals and was approved by the university committee on use and care of animals at the university of michigan. If you find an inhibitor of this protein kinase, you should be able to obtain the same effect as knocking out the gene. Timothy blackwell and fiona yull of the vanderbilt university school of medicine also are co-authors. Saltiel’s team is now searching for small molecules that block ikke protein-kinase activity. If successful candidates are identified and drug development is pursued, a new treatment for obesity and diabetes is likely a decade away, he said.
In that situation, the ikke protein kinase acts as a brake on the metabolism. Protein kinases are enzymes that turn other proteins on or off.