A research team headed by Professor Helena Edlund at Ume University has achieved a breakthrough in our understanding of how obesity causes increased levels of insulin, sugar, and blood fats leading to diseases like type-2 diabetes and liver degeneration. The findings also indicate a direct way to prevent these diseases.

Today obesity is epidemic in the industrialized world, causing disturbances in blood levels of insulin, sugar, and blood fats that lead to high blood pressure, type-2 (adult onset) diabetes, and fatty liver, which in turn conspire to cause cardiovascular disorders, the leading cause of premature death in the Western world. Obesity is also associated with an increased risk of various types of cancer. Children and adolescents are becoming more and more obese and are also developing these complications. In the U.S. this has meant that the next and coming generations may be the first in modern history to be sicker and a shorter lifespan than their parents, which is considered a medical disaster.

Today we do not understand at the molecular level how obesity causes diabetes, fatty liver, and blood-fat disturbances, and we therefore also lack effective methods of treatment to prevent or cure these complications. A research team led by Helena Edlund at Ume University is now publishing in the journal Cell Metabolism a breakthrough in our understanding of the role of obesity in this connection. Her associate at Ume University is post-doctoral fellow Pr Stenberg, and other co-authors belong to Dr. Michael D. Walker's team at the Weizman Institute of Science, Israel.

Obesity leads to heightened levels of free fatty acids that are stored and converted to fats in various tissues. A recently discovered surface receptor for free fatty acids, called GPR40, is in mice present solely in the insulin-producing beta cells. Mice, like humans, that eat a diet rich in calories gain weight quickly and experience disturbances in their blood level
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Contact: Hans Fllman
hans.fallman@adm.umu.se
46-90-786-6465
Swedish Research Council
12-Apr-2005

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