B. Kahn, chief of the division of endocrinology, diabetes, and metabolism at Beth Israel Deaconess Medical Center in Boston.

Type 2 diabetes develops as the result of insulin resistance, a condition defined by the body's inability to properly utilize naturally produced insulin for the breakdown of sugars, starch and other glucose-rich foods into energy. The resulting dangerous buildup of glucose and insulin in the blood is also associated with a high risk for cardiovascular disease.

Noting that insulin resistance seems to go hand-in-hand with reduced levels of the glucose transporter protein, the researchers used specially bred mice to look for a causal relationship between levels of RBP4 and other fat-cell proteins. After eliminating a range of alternate molecular options, they observed that levels of glucose-carrying proteins fell as fat cell RBP4 production rose.
Further tests in both mice and humans confirmed that excess production of RBP4 appears to promote a drop in the glucose-carrying proteins. Insulin resistance, they concluded, might therefore be avoided if RBP4 levels could be reduced and controlled. Kahn's team reported the findings in the July 21 issue of Nature.