Sweet lumps

Diabetes and obesity are related

 
Last Updated: Saturday 04 July 2015

obesity and diabetes are related at the molecular level, researchers at Beth Israel Deaconess Medical Center (bidmc), usa have found out. They have identified a mechanism that helps explain how the hormone leptin acts to metabolize fatty acids in muscle, establishing for the first time a novel molecular link between obesity and diabetes. This revelation could help create the possibility of a new target for the development of drugs to help manage both conditions.

Discovered in 1994, leptin first gained widespread attention as a 'satiety signal' or appetite suppressant. Initial studies revealed that the hormone, which is produced in fat cells, travels through the bloodstream and interacts with receptors in the brain to provide a 'signal' that the body has consumed enough food and should stop eating.

However, scientists since then have demonstrated that leptin's role is not confined to suppressing appetite. Leptin receptors have also been identified in the T-cells of the immune system and in new blood vessels, and as this new research suggests, the hormone has also been shown to play an important role in metabolism.

"Leptin is a master regulator of our bodies' hormonal systems," explains Barbara Kahn, chief of endocrinology at Beth Israel Deaconess and Professor of Medicine at the Harvard Medical School. "It probably evolved as a regulator that could be suppressed to protect people and animals when no food was available." Kahn served as the study's senior author. Impaired fuel metabolism is a well-known factor in obesity as well as type 2 diabetes. When fatty acids in muscle and the liver are not sufficiently utilised, their buildup not only impairs the body's ability to burn calories, but also leads to insulin resistance, which increases a person's risk of developing diabetes. This new research focuses on an enzyme that had previously been identified as a 'fuel gauge', which acts on other key enzymes in both cholesterol metabolism and glycogen synthesis. Kahn and her colleagues hypothesised that the enzyme might also be serving as a signaling pathway for leptin, enabling the hormone to metabolize fatty acids in muscle.

To test their hypothesis, the researchers injected laboratory mice with leptin. They discovered that the hormone was indeed activating particular enzyme in muscle when administered either directly into a peripheral vein or into the brain's hypothalamus. This novel effect was the same in experiments conducted outside the body, when muscle was removed from the mice and incubated with leptin. In addition, by blocking the nerves to the animals' legs, the researchers showed that leptin was exerting an indirect effect on muscle by way of the brain and sympathetic nervous system.

These results demonstrated that at first there was an early activation of the enzyme because of leptin's direct effect on skeletal muscle. But later more sustained, activation was indirectly taking place via the central nervous system. Together with results of an earlier study showing that mice grew very lean when the enzyme was removed, these findings suggest that this pathway could be a particularly promising target for drug treatments for obesity and diabetes.

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