Researchers from Japan report that S-1-propenyl-L-cysteine, a molecule found in aged garlic extract, counteracted frailty and muscle weakness in elderly mice via the activation of a newly identified signaling cascade. These findings were detailed in the journal Cell Metabolism.
Historically, garlic (Allium sativum) has been employed across the globe for the treatment of numerous ailments and health concerns. In ancient Egypt, Greece, China, and India, it was traditionally utilized as a universal remedy to boost vitality, stamina, and combat infections.
More recently, a growing body of scientific evidence supports the substantial positive health effects derived from garlic itself and aged garlic extract (AGE).
Several biologically active constituents have been isolated, including allicin from fresh garlic, alongside S-allyl-L-cysteine (SAC) and S-1-propenyl-L-cysteine (S1PC) present in AGE.
Among these, S1PC, a sulfur-containing amino acid relatively abundant in AGE, has lately been subjected to thorough scrutiny, demonstrating a range of intriguing pharmacological activities such as enhancing mitochondrial energy metabolism, ameliorating atherosclerosis, and protecting vascular endothelial cells.
“During my clinical work as a physical therapist, I was often distressed seeing elderly individuals lose physical function and vigor simply because they didn’t suffer from a specific, diagnosable medical condition. This void in preventative care motivated my investigation,” explained Kiyoshi Yoshioka of the Research Center for Promoting Productive Longevity and the National Center for Geriatrics and Gerontology. “We hope our findings can contribute to improving physical fitness and muscle strength in the aged through the simple integration of this nutraceutical into their daily diet.”
In their investigation, Yoshioka and his team observed that S1PC stimulates the enzyme liver kinase B1 (LKB1), a crucial coordinator of cellular metabolism.
Significantly, S1PC promotes the formation of a protein complex involving LKB1, which subsequently leads to the activation of the SIRT1 pathway, thus facilitating the secretion of extracellular NAMPT (eNAMPT) from adipose tissue.
The enzyme eNAMPT is essential for the synthesis of NAD+, a small but vital molecule involved in cellular defense, DNA repair, and energy generation.
Instead of directly influencing muscle tissue, eNAMPT is packaged within extracellular vesicles (eNAMPT-EVs) released from fat tissue. These vesicles travel through the bloodstream to target the hypothalamus, a central regulatory hub within the brain.
This interaction is linked to an increase in sympathetic nerve signaling, which, in turn, results in improved muscle function.
These discoveries illuminate a novel communication axis connecting adipose tissue, the brain, and skeletal muscle, offering new avenues for understanding how age-related functional decline might be regulated.
The functional benefits afforded by S1PC were further validated using older mouse models.
Sustained administration of S1PC was shown to reduce frailty scores, boost the force-generating capacity of skeletal muscles, and restore normal body temperature.
Notably, a parallel human study indicated that S1PC elevates circulating levels of eNAMPT, particularly in individuals possessing adequate fat reserves.
The fact that the effect of S1PC on eNAMPT-EV secretion remains consistent across cells, mice, and humans underscores its potential utility as an anti-aging agent in human application.
“Our results demonstrate a previously unrecognized and unique role for S1PC in activating LKB1 and fostering inter-organ communication that mitigates muscle weakness,” stated Shin-ichiro Imai of the Research Center for Promoting Productive Longevity. “We surmise that S1PC likely possesses broader rejuvenating effects that warrant in-depth exploration.”
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