A protein released by fat cells acts as a link between obesity and type 2 diabetes and could be a possible target for drug developers.

People with type 2 diabetes have high levels of the protein, called retinal binding protein 4 or RBP4, according to previous studies.

Researchers in the U.S. found when the protein is released by fat tissue in mice, insulin resistance results. In insulin resistance, the body does not use insulin properly to convert glucose to energy.

"Being resistant to insulin is one of the major causes of diabetes," said Dr. Barbara Kahn, an endocrinology researcher at the Beth Israel Deaconess Medical Center in Boston, Mass.

People with type 2 diabetes do not make enough insulin, or their muscle, fat and liver cells may not use it properly.

Kahn and her colleagues found higher levels of RBP4 caused insulin resistance while lower levels helped relieve insulin resistance in mice genetically engineered for the research.

Diabetes researchers have tested various substances in fat such as the hormone leptin, looking for a link between insulin resistance and a glucose transporter protein. None has panned out but RBP4 appears to fit the bill.

The protein therefore might be a target for developing anti-diabetic therapies, Kahn said.

The study appears in Thursday's issue of the journal Nature.

In a commentary accompanying the study, scientists agreed a substance involved in moving fat like RBP4 "represents a possible drug target with the potential to uncouple insulin resistance from obesity."

To explain why, Deborah Muoio and Christopher Newgard suggest insulin resistance in fat cells may be an early consequence of obesity. It's as if fat cells mistake obesity for starvation in how they act, they said.

Kahn's finding "moves the [fat cell] and its secreted factors closer to the epicentre of the diabetes and obesity epidemic," wrote the nutrition and metabolism researchers at Duke University Medical Center in Durham, N.C.