Transplanting the fat-burning pathway of bacteria into mice allowed the rodents to eat a high-fat diet while remaining lean. And the results of the study point to a whole new approach to treating ailments in humans who could benefit from some other species' biologic functions.
Senior author James Liao said that the scientists concentrated on the glyoxylate shunt, a pathway made of two enzymes that a cell in bacteria uses to convert fat to sugar. Liao believes that humans don't have this mechanism because our bodies have been conditioned to store fat rather than burn it.
By introducing the genes for the enzymes into human cells, the scientists found that the new mechanism didn't convert fat, it burned it away entirely. The genes triggered a cellular response that caused cells to metabolize fat. The team then transplanted the genes into mice livers and found that normal mice became fat while the genetically engineered mice "remained skinny despite the fact that they ate about the same and produced the same waste."
- read the story in MIT Technology Review