Proteins that shuttle lipids in the body might be a missing link between obesity and other conditions that tend to go along with the excess weight, including diabetes and fatty liver disease, according to Harvard School of Public Health researchers reporting in the journal Cell Metabolism.

The constellation of obesity and its related symptoms, commonly referred to as metabolic syndrome, is estimated to affect more than one out of every five adults in the United States.

Mice lacking two related fatty acid binding proteins (FABPs), aP2 and mal1, exhibited striking changes in their lipid profiles and strong resistance to diet-induced obesity, insulin resistance, type 2 diabetes, and fatty liver disease, the researchers reported.

Mice deficient for both proteins gained less weight than normal mice when fed a high-fat diet due to an increase in energy expenditure and resulting 25 percent reduction in total body fat, they found. Mice lacking the FABPs also exhibited significant shifts in the distribution of fatty acids in fat, muscle, and liver.

Mutant animals on the high-fat diet had significantly lower blood glucose and insulin levels than normal mice on the same diet. Rising blood glucose and insulin concentrations in overweight animals are an indicator of obesity-induced insulin resistance and type 2 diabetes. Examination of livers from the mutant mice also revealed a striking reduction in the infiltration of fat, in comparison to the livers of normal mice.

The current findings--together with the team's earlier discovery of the proteins' role in atherosclerosis--suggest that the FABPs have a robust impact on multiple components of metabolic syndrome by integrating metabolic and inflammatory responses in mice. The researchers further propose that the proteins may serve as a powerful target for the treatment of obesity, diabetes, and cardiovascular disease.

Other sources: Cell Metabolism