Dr. Philip Wood, professor in Sanford-Burnham’s Diabetes and Obesity Research Center at Lake Nona, Florida, co-authored a study showing that obesity-resistant mice could be genetically engineered by deleting an enzyme that helps break down fatty acids. The study, which appeared May 5 in the journal Cell Metabolism, was co-led by Dr. Wood and Dr. Gerald Shulman of the Howard Hughes Medical Institute and Yale University.

In the study, mice lacking the gene – called VLCAD – were fed a high-fat diet. Since VLCAD is necessary for normal fatty acid metabolism and the production of cellular energy, the scientists figured that disrupting the gene’s function would inhibit metabolism and lead to weight gain and other ailments. However, instead of packing on extra fat, the mice were actually protected from obesity and insulin resistance (an early stage  of type 2 diabetes). The researchers think that VLCAD deficiency triggers a back-up mechanism that acts like an emergency generator, compensating for the loss of the enzyme.

“This study illustrates the power of a genetic mouse model to tease apart different components of the fat burning process and insulin resistance, a common side effect of obesity,” Dr. Wood explained. “By inactivating this one step in fat burning, we activated two different drug targets currently used to treat problems of excess fat in human patients.”

Dr. Wood was also interviewed in a recent story about obesity by WJRT-TV, the ABC affiliate in Flint, Michigan.