A new theory has been suggested that the reduction of membrane fluidity in muscle cells is the cause of sarcopenia, which reduces muscle volume and strength.
The Korea Institute of Biotechnology announced that its research team led by Kwon Ki-sun, a researcher specializing in aging control, published the results in the online edition of Nature Communications (IF12.121), an international journal in biology, on the 9th of last month.
As aging progresses, the amount and strength of muscles decrease, which is called senile muscular dystrophy. Chronic inflammation, hormonal imbalance, malnutrition, reduced stem cells, and decreased mitochondrial function are deemed main causes.
In 2014, Dr. Kwon’s team, with the team led by Dr. Lee Chul-joo of the Korea Institute of Science and Technology (KIST), analyzed the protein content of aging muscles and found a change in the lipid protein called FABP3.
Dr. Kwon’s team also confirmed that, through lipidomics, the saturated fatty acid chain is increasing during the phospholipid composition of the endometriosis in aging muscles with the research team led by Dr. Hwang Jang-sook of the Korea Basic Science Institute (KBSI).
The research team analyzed the results of the two studies and concluded that the increased lipid transfer protein (FABP3) due to aging increases the saturated fatty acid chain of the endometrium, causing fluid reduction, stress in the parcel body, which reduces muscle mass and muscle strength.
This means that artificially inhibiting the lipid transfer protein (FABP3) reduces the saturated fatty acid chain among membrane components, then increases membrane liquidity, and recovers the stress of the parcel body, turning aging muscles to youth.
Endoplasmic reticulum is an organelle that controls muscle mass and muscle strength, and is the membrane structure that contributes the muscle the most among all biological tissues.
“The increase in FABP3 increases the saturated fatty acid chain of the endometriosis and, on the contrary, artificially inhibited FABP3 reduces the saturated fatty acid chain,” a team official said. “This allowed us to suggest that FABP3 is an age-related lipid protein.”
The research team used the method of fluorescence recovery after photobleaching (FRAP) to observe in real time that membrane liquidity decreases as the saturated fatty acid chain increases, and to identify the role of membrane fluidity in controlling the EP stress signal.
In an experiment using an old mouse, the team observed that the amount of muscle as well as muscle strength increases when artificially inhibiting the expression of the muscle’s lipid transmission protein (FABP3).
Through this, the research team proposed the “fluidity of aging” theory that a “biological” clock called gene expression with age would cause a “chemical” change in biological membrane lipid components, which in turn would regulate the fluidity of the membrane, which is “physical” and ultimately contribute to the constancy.