- Sarcopenic obesity is a condition associated with obesity and age-related muscle loss.
- Sarcopenic obesity can reduce quality of life and increase the risk of hospitalization and death. There is also a shortage of cures for this condition.
- A new study in mice has shown that a drug called BAM15 can prevent loss of skeletal muscle mass and function and prevent weight gain.
- This study suggests that BAM15 achieved this by reducing inflammation and improving the function of mitochondria, the driving force of cells.
Recent studies published in
The study found that BAM15 was effective in combating disorders associated with sarcopenic obesity, including increased energy expenditure, reduced inflammation, and improved mitochondrial function in mice.
Christopher Axelrod, a researcher at the Pennington Center for Biomedical Research, who co-authored the study, said: Today’s medical news:
“Sarcopenic obesity is a debilitating disease and no targeted therapies are currently available. This therapeutic approach provides first evidence that sarcopenic obesity can be treated by reducing the efficiency of energy production.”
Axelrod said the results of this study could be important in purifying / developing effective and safe medicines for humans.
Sarcopenia
Sarcopenia associated with obesity is known as sarcopenia obesity and is worse than sarcopenia and obesity alone. Specifically, sarcopenic obesity is associated with a much more rapid decline in physical function and an increased risk of cardiovascular disease, hospitalization, and death.
Sarcopenic obesity is associated with reduced energy expenditure rather than overdose of calories. Therefore, treatments that can increase energy expenditure may help fight sarcopenic obesity.
Obesity and sarcopenia share a common biological mechanism, including mitochondrial dysfunction in skeletal muscle cells. Mitochondria are organelles within cells that are involved in energy production and are important for muscle function.
Energy production in mitochondria consists of two different processes that are bound to each other, and the binding of these two processes determines the efficiency of energy production.
Studies have shown that the uncoupler of two processes using a drug called a mitochondrial uncoupler
The
To assess the effect of BAM15 on sarcopenic obesity, researchers used aged mice that maintained a high-fat diet and were treated with BAM15 for 10 weeks. The control group consisted of animals fed a high-fat diet that did not contain BAM15 and showed weight gain during the study period.
Both the control and BAM15 animals did not have different food intakes, but the animals treated with BAM15 did not show weight gain, unlike the control group. Mice treated with BAM15 had lower body fat levels than control animals, which may be the cause of the lack of weight gain.
Mice treated with BAM15 had greater muscle mass and strength than control animals. This suggested that mitochondrial decoupling maintains muscle mass and function.
In addition, BAM15 treatment resulted in higher physical activity and energy expenditure levels.
Next, the researchers evaluated the effect of BAM15 on the underlying biological processes of sarcopenic obesity.
Chronic mild inflammation
Researchers have found that BAM15 treatment reduces markers of local and systemic inflammation of skeletal muscle.
Similarly, reduced mitochondrial function and a reduced number of healthy mitochondria are characteristic of age-related muscle loss. Researchers have found that BAM15 improves mitochondrial function, enhances the production of new mitochondria, and promotes the removal of damaged mitochondria.
Muscle wasting in sarcopenia with aging is also associated with increased proteolysis and accumulation of misfolded proteins.
A protein is made up of one or more chains of amino acids that are folded into a particular shape.
Researchers have found that treatment with BAM15 in aged mice reduces the expression of markers associated with protein misfolding and degradation, cell stress, and cell death in skeletal muscle tissue.
Dr. John Kirwan, co-author of the study and managing director of the Pennington Center for Biomedical Research, said: MNT:
“This study provides first evidence that the mitochondrial uncoupler BAM15 prevents skeletal muscle obesity with increased adipose tissue or age-related muscle loss. The study provides older mice (humans). It was done at (equivalent to 65 years old). “
Dr. Kirwan said more research is needed to determine if the treatment is effective for humans.
“”[T]His findings have important implications for improving the quality of life of the elderly, especially for the rapidly increasing obese people. By preventing, delaying, or reversing the causes and consequences of sarcopenic obesity, people may be able to lead longer and healthier lives. “
—Dr. John Kirwan, Research Co-author
