LOS ANGELES, June 8 (UPI) -- U.S. researchers have engineered a metabolic pathway in mice to prevent diet-induced obesity.
The UCLA scientists led by Professor James Liao and Associate Professor Katrina Dipple constructed a non-native pathway in mice that increased fatty acid metabolism and resulted in resistance to diet-induced obesity.
Graduate student Jason Dean, the study's author, said the idea came from plants and bacteria.
"We know plants and bacteria digest fats differently from humans, from mammals," Dean said. "Plant seeds usually store a lot of fat. When they germinate, they convert the fat to sugar to grow. The reason they can digest fat this way is because they have a set of enzymes that's uniquely present in plants and bacteria. These enzymes are called the 'glyoxylate shunt' and are missing in mammals."
Liao's team cloned bacteria genes from Escherichia coli that would enable the shunt, then introduced the cloned E. coli genes into the mitochondria of liver cells in mice; mitochondria are where fatty acids are burned in cells.
The researchers found the glyoxylate shunt cut the energy-generating pathway of the cell in half, allowing the cell to digest the fatty acid much faster than normal. They also created an additional pathway for converting fatty acid into carbon dioxide.
The study is detailed in the journal Cell Metabolism.