Cause of Sarcopenia in the Elderly: "Decrease in Makyudongseong"

New Theory Proposed on Causes of Sarcopenia in Elderly
Expected Applications in Anti-Aging and Rejuvenation Drug Development

It has been found that people living alone have a higher probability of developing dementia. Photo by Getty Images Bank

[Asia Economy Reporter Junho Hwang] A new theory has been proposed that a decrease in the membrane fluidity of muscle cells is the cause of age-related sarcopenia.

Dr. Kwon Gi-seon’s research team at the Korea Institute of Life Science and Biotechnology's Aging Control Research Division presented this theory and recently published their findings in the international journal Nature Communications, the team announced on the 22nd.

As the human body ages, both the quantity and strength of muscles decrease. This condition is called age-related sarcopenia, and since 2016, the World Health Organization has assigned a disease code to this condition. Causes of age-related sarcopenia have been identified as chronic inflammation, hormonal imbalance, nutritional deficiency, stem cell reduction, and mitochondrial dysfunction.

However, based on previous research results, the team pointed to a decrease in the membrane fluidity of muscle cells as the cause of age-related sarcopenia. They explained that lipid transport protein (FABP3), which increases with aging, raises the saturated fatty acid chains in intracellular membrane components, reducing membrane fluidity and causing stress to the endoplasmic reticulum, which in turn lowers muscle mass and strength. The endoplasmic reticulum is an intracellular organelle that regulates protein synthesis controlling muscle mass and calcium signaling controlling muscle strength. Among all biological tissues, it plays a significant structural and functional role in muscles.

The research team also provided evidence that artificially inhibiting FABP3 reduces the saturated fatty acid chains in membrane components, increases membrane fluidity, and relieves stress on the endoplasmic reticulum, thereby rejuvenating aged muscles. In experiments using aged mice, they artificially suppressed the expression of the lipid transport protein (FABP3) in muscles and observed increases not only in muscle mass but also in muscle strength.

Regarding these research results, the team stated, "The significance lies in proposing an original 'fluidity theory of aging,' which suggests that the 'biological' clock of gene expression over time induces 'chemical' changes in membrane lipid components, which in turn regulate the 'physical' fluidity of the membrane, ultimately contributing to 'physiological' homeostasis."

Dr. Kwon Gi-seon said, "This theory is expected not only to be broadly applied as a principle of aging in various biological organs but also to be utilized in the development of new drugs that slow down or reverse the aging clock."