Researchers have found that the hormone, ghrelin, may help protect the elderly population from muscle loss. The study, presented at e-ECE 2020 online conference on Tuesday, found that administering a particular form of ghrelin to older mice helped to restore muscle mass and strength.
“As muscle-related diseases are a serious health concern in the elderly population, these findings suggest a potential new treatment strategy for muscle loss to enable the ageing population to remain fit and healthy,” said study author from University of Piemonte Orientale in Italy.
Ghrelin is a hormone involved in metabolic regulation and energy balance through activation of appetite, but also plays an important role in protecting against muscle wasting.
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According to the researchers, both acylated (AG) and unacylated (UnAG) forms are present in the body, but UnAG does not bind to the AG receptor (GHSR-1a), so does not increase appetite.
A growing body of evidence indicates that UnAG is acting at an unidentified receptor, which also mediates some common AG and UnAG biological activities, including a strikingly protective effect against muscle wasting. “Ghrelin levels decline as we age and may be involved in the development of sarcopenia, but the role of AG versus UnAG in this process has not been investigated previously,” the team wrote.
For the current study, the research team investigated how unAG affected the age-related decline of muscle mass and function, by either deleting the ghrelin gene in mice or overexpressing unAG.
Muscle function as they aged was assessed through a wire hanging test, during which “falling” and “reaching” scores were recorded, to assess whole-body strength and endurance. Both the deletion of the ghrelin gene and the lifelong over expression of UnAG reduced age-associated decline in muscle mass and function.
Despite both groups of animals displaying similar ageing tendencies in body weight and muscle mass, the mice overexpressing UnAG maintained better muscle structure, performance and metabolism, more typical of muscle in younger mice.
The study indicates that UnAG, or possibly drugs that mimic it, can preserve muscle function and reduce the risk of age-related sarcopenia, without causing weight gain and obesity.The research team now plans to identify the receptor mediating UnAG biological activities. This will help better define the molecular pathways involved in AG/UnAG actions and to design treatments that may reduce the loss of muscle mass in sarcopenia and other similar conditions. (IANS)