Potential therapeutic target for muscle atrophy identified

June 12th, 2009 - 4:37 pm ICT by ANI  

Washington, June 12 (ANI): Researchers from University of Piemonte Orientale, Novara, Italy have identified a potential therapeutic target for common problem of muscle atrophy.

The condition results in an extensive loss of muscle mass and function, which greatly worsens quality of life and occurs in diseases such as cancer, diabetes, AIDS and heart failure, negatively affecting the patients’ prognosis.

Muscular atrophy can occur with aging, inadequate food intake such as in anorexia nervosa, or disuse (in those who are bedridden or who must keep a limb immobile)/

Presently there are few options to treat the problem such as anabolic steroids (testosterone) and insulin-like growth factor 1 (IFG-1).

However, there are concerns over its safety and effectiveness, said Dr Andrea Graziani, molecular biologist with the Department of Clinical and Experimental Medicine and the Biotechnology Centre for Applied Medical Research, University of Piemonte Orientale, Novara, Italy.

“Because of the wide impact of muscular atrophy on public health, it is of pivotal importance to find new and better drug strategies to treat it,” Graziani added.

The research team focused their study on des-acyl ghrelin, a form of ghrelin, the appetite-stimulating hormone found in the body.

Until recently, researchers thought that des-acyl ghrelin was inactive because it does not share the main activities of the hormone.

In the new study, they have found that des-acyl ghrelin shares some biological activities with ghrelin, such as stimulating differentiation of other cells, including cells that are precursors to skeletal muscle cells.

The study conducted on mice showed that des-acyl ghrelin has a direct anti-atrophic activity on the skeletal muscle of mice with muscular atrophy caused by either denervation (nerve injury) or fasting.

The mice that were genetically altered to have increased levels of des-acyl ghrelin had less skeletal muscle loss than the untreated control mice. This held true for both causes of muscular atrophy.

The results were presented at The Endocrine Society’s 91st Annual Meeting in Washington, D.C. (ANI)

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