A new study in the September issue of Cell Metabolism, a publication of Cell Press, points to a new method for burning off all those irresistible extra calories—by turning on an energy-draining, but otherwise futile, cycle of protein synthesis and breakdown.
Christopher Lynch of The Pennsylvania State University College of Medicine and his colleagues found that they could drive such heightened protein turnover in mice by disrupting an enzyme involved in the metabolism of some amino acids, the building blocks of proteins. The enzyme-deficient animals showed elevated blood levels of the essential amino acid leucine, an important nutrient signal, and became slimmer than normal mice despite eating more food. They also showed “remarkable” improvements in glucose and insulin tolerance, and resistance to becoming obese on a high-fat diet.
“The mice on the outside look normal, just skinnier and smaller,” Lynch said. “After looking at their metabolism, we found that for the same activity, they were using more energy.”
Moreover, the researchers found that the animals that ate the most food also expended the most energy. “That would be ideal for people who are overweight,” Lynch said. “They could continue to eat and just waste the energy and be thin.”
Abundant food supplies and a sedentary lifestyle have contributed to the current epidemic of obesity in Western nations, the researchers said. Obesity results when people consume more energy in their diet than they expend. In both short-term and relatively long-term studies, high-protein and low-fat diets have been found to increase energy expenditure, they noted, while short-term protein intake helps stave off hunger.
The effects of dietary protein are thought to be driven at least in part by leucine and perhaps other so-called branched-chain amino acids (BCAAs). Yet it has remained unclear whether leucine supplementation actually improves or worsens obesity, Lynch said.