As long as physicians do not know on the molecular level how obesity causes diabetes, fatty liver, and blood-fat disturbances, they lack effective methods of treatment to prevent or cure these complications.
A research team led by Helena Edlund at Umeå University is now publishing in the journal Cell Metabolism a breakthrough in our understanding of the role of obesity in this connection.
Obesity normally 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 levels of insulin, sugar, and fats, and they develop fatty liver and diabetes.
The findings of the Umeå team show that mice that lack GPR40 receptors are healthy and experience normal weight gain on a calorie-rich diet. These mice are, however, protected from the complications and diseases that obesity provokes.
The findings thus indicate that obesity leads to increased levels of free fatty acids that stimulate the secretion of insulin via GPR40 receptors, which in turn contributes to disease development. By inactivating GPR40 function the animals are protected from these diseases.
This theory is supported by the finding that mice with an increased number of GPR40 receptors on their beta cells develop diabetes. GPR40 belongs to the class of receptors targeted by most drugs. The receptors also occur on human beta cells, and therefore substances that block these receptors are prime candidates as drugs for preventing or curing diabetes and other complications of obesity.
MEDICA.de; Source: Umeå University