U.S. researchers at Washington University School of Medicine in St. Louis have identified a potential target for treating diabetes and obesity, according to a study published online on Thursday in the journal Cell Metabolism.
Studying mice, the researchers found that when the target protein was disabled, the animals became more sensitive to insulin and were less likely to get fat even when they ate a high-fat diet that caused their littermates to become obese.
They studied how the body manufactures fat from dietary sources such as carbohydrates. That process requires an enzyme called fatty acid synthase (FAS). Mice engineered so that they don't make FAS in their fat cells can eat a high-fat diet without becoming obese.
"Mice without FAS were significantly more resistant to obesity than their wild-type littermates," said first author Irfan Lodhi. "And it wasn't because they ate less. The mice ate just as much fatty food, but they metabolized more of the fat and released it as heat."
To understand why that happened, the researchers analyzed the mice's fat cells. Mice have two types of fat: white fat and brown fat. White fat stores excess calories and contributes to obesity. Brown fat helps burn calories and protects against obesity.
In mice genetically blocked from making fatty acid synthase in fat cells, the researchers noticed that the animals' white fat was transformed into tissue that resembled brown fat.
