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Source: Anti-Aging News  Sep 08, 2020  3 years, 5 months, 2 weeks, 2 days, 6 hours, 9 minutes ago

Anti-Aging News: Hormone Ghrelin Can Prevent Sarcopenia And Restore Muscle Loss In The Elderly According to Italian Study

Anti-Aging News: Hormone Ghrelin Can Prevent Sarcopenia And Restore Muscle Loss In The Elderly According to Italian Study
Source: Anti-Aging News  Sep 08, 2020  3 years, 5 months, 2 weeks, 2 days, 6 hours, 9 minutes ago
Anti-Aging News: A new study involving a collaboration of Italian researchers from 11 medical universities and institutes and also the Stem Cell Institute At Leuven-Belgium indicates that the hormone, ghrelin, may help protect the elderly population from muscle loss.

The study which involved administering a particular form of ghrelin to older mice saw muscle mass and strength being restored.
The study was presented at the recent online 22nd European Congress of Endocrinology or e-ECE 2020 and is also published in the journal: Aging.
Muscle-related diseases are a growing serious health concern in the elderly population often causing debilitating conditions.
The study findings suggest a potential new treatment strategy for muscle loss to enable the aging population to remain fit and healthy.
Sarcopenia or age-related skeletal muscle mass loss in absence of any underlying disease, is defined often which to deterioration of elderly people's quality of life. It results in a decline in muscle mass and functionality, often resulting in poor balance, higher risk of falls or fractures, immobilization and loss of independence.
The hormone Ghrelin is involved in metabolic regulation and energy balance through activation of appetite, but also plays an important role in protecting against muscle wasting.
It is known that both acylated (AG) and unacylated (UnAG) forms of the hormone are present in the body, but UnAG does not bind to the AG receptor (GHSR-1a), so does not increase appetite.
Emerging studies and data 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.
It is known that 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.
Researchers from the University of Piemonte Orientale in Italy led by Dr Emanuela Agosti, along with researchers from other institutions investigated how unAG affected 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.
It was found that the deletion of the ghrelin gene and the overexpression of UnAG reduced age-associated decline in muscle mass and function.
However despite both groups of animals displaying similar aging 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.
Dr Agosti told Thailand Medical News, “Understanding the causes and effects of sarcopenia will improve our ability to prevent, detect, and hopefully manage this disease. These study findings provide novel understanding and poi nt to UnAG, or analogues, as a possible therapeutic target for future treatment."
The research 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.
Dr Agosti further added, "Due to the worldwide increase in the elderly population, sarcopenia has an important social impact greatly affecting both aged people's quality of life and government health care costs. Therefore, therapeutic strategies aimed at preventing and/or reducing sarcopenia are of pivotal importance."
The study team 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 specific treatment protocols that may reduce loss of muscle mass in sarcopenia and other similar conditions.
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