Scientists at the Weizmann Institute of Science in Rehovot and the University of Umea in Sweden have unraveled a mechanism by which fat contributes to the onset of the Type 2 diabetes, which affects one out of 12 adults in the Western world and threatens to double in the next two decades, The Jerusalem Post reported.

To understand the role of GPR40, a receptor found on the outer surface of pancreatic beta cells, Prof. Michael Walker and students Nir Rubins and Reut Bartoov-Shifman of the Rehovot institute's biological chemistry department teamed up with Prof. Helena Edlund and post-doctoral fellow Dr Per Steneberg of Umea.

Together, they developed two types of lab mice with modified GPR40 activity. In the first, the scientists used a technique known as gene knock-out to prevent production of the GPR40 receptor. The second type had overactive GPR40 genes creating a surfeit of fat-signaling receptors that tricked the beta cells into sensing high fatty acid levels, even on a normal diet.

Throughout the trial, the GPR40 knock-out mice remained healthy, apparently suffering no ill-effects from the deletion of the receptor, even when the fat content of their diet was raised substantially. In contrast, normal mice on a high-fat diet displayed typical symptoms of the first stage of diabetes. But strikingly, in the animals with extra GPR40 receptors, the disease progression was swift: They soon began to exhibit the classic symptoms of full-blown diabetes, including failure of the beta cells to produce adequate amounts of insulin.

Walker explained: "These studies show that excessive GPR40 action can trigger each of the two stages of the disease. "Our results establish GPR40 as an important link between obesity and diabetes. This gives us a new tool to combat the diabetes epidemic: For example, it might be possible in the future to treat the condition using drugs that block the action of this receptor."

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