A new form of treatment has been identified for offering relief to patients suffering from muscle atrophy, as per the results of an animal study presented at the Endocrine Society’s 91st Annual Meeting in Washington, D.C.

It was remarked by study co-author Andrea Graziani, PhD, molecular biologist with the Department of Clinical and Experimental Medicine and the Biotechnology Center for Applied Medical Research, University of Piemonte Orientale, Novara, Italy, that present-day recommended options such as anabolic steroids (testosterone) and insulin-like growth factor 1 (IFG-1) may not be classified as safe.

From News-Medical.Net:

“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 said.

Graziani and his co-workers are studying 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 ghrelin-stimulating appetite, fat and the release of growth hormone.

However, Graziani’s group recently found that des-acyl ghrelin shares some biological activities with ghrelin, such as stimulating differentiation of other cells, including-important to these study-cells that are precursors to skeletal muscle cells.

In this new study, the researchers discovered 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. 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 mechanism by which des-acyl ghrelin protects muscle against atrophy is not yet known, the authors reported. However, it is distinct from the action of anabolic steroids and IGF-1.

It was noted by the involved researchers that this hormone, which is known to stimulate appetite, poses a direct anti-atrophic activity on mice’s skeletal muscle caused by fasting or nerve injury.