MOTS-c Peptide Information
| Molecular formula: | C101H152N28O22S2 |
| Molecular weight: | 2174.6 g/mol |
| PubChem CID: | 146675088 |
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What is MOTS-c?
MOTS-c (mitochondrial open reading frame of the 12S rRNA type-c) is a 16-amino acid peptide encoded by the mitochondrial genome that has emerged as a promising subject in biomedical research. Discovered in 2015, MOTS-c has been found to play important roles in regulating metabolism, insulin sensitivity, and energy homeostasis. Research has shown that MOTS-c can improve glucose metabolism in skeletal muscle, reduce obesity, and potentially delay age-related physical decline.
MOTS-c has been studied for its potential therapeutic applications in various conditions, including diabetes, cardiovascular diseases, and age-related disorders. Notably, MOTS-c levels in plasma tend to decrease with age, suggesting its relevance to the aging process. As research continues, MOTS-c represents an exciting avenue for understanding mitochondrial-nuclear communication and developing novel interventions for metabolic and age-related diseases.
MOTS-c and Metabolism
Research has shown that MOTS-c treatment can boost glucose uptake in skeletal muscle and improve insulin sensitivity. This could be beneficial for those studying type 2 diabetes or insulin resistance [R, R].
MOTS-c also appears to influence lipid metabolism. Experiments have revealed that MOTS-c promotes fat utilization and increases lipid oxidation capacity in cells. This effect on lipid metabolism may contribute to MOTS-c’s potential in preventing diet-induced obesity and improving metabolic flexibility [R, R].
Interestingly, MOTS-c has been found to activate the AMPK pathway, a key regulator of cellular energy homeostasis. This activation of AMPK by MOTS-c leads to increased glucose uptake, enhanced fatty acid oxidation, and improved mitochondrial function. The peptide’s ability to modulate AMPK signaling underscores its importance in maintaining metabolic balance [R, R]
Research has also indicated that MOTS-c levels in the body are responsive to exercise. Studies have shown that endogenous MOTS-c levels increase significantly in skeletal muscle following physical activity, suggesting a potential role for MOTS-c in exercise-induced metabolic adaptations [R].
Furthermore, MOTS-c has been implicated in regulating mitochondrial metabolism. The peptide appears to influence the tricarboxylic acid (TCA) cycle, acylcarnitine shuttle, and urea cycle, all of which are critical for cellular energy production and waste removal. This regulation of mitochondrial metabolic pathways may contribute to MOTS-c’s overall effects on systemic metabolism [R].
In the context of aging and age-related metabolic disorders, MOTS-c shows promise as a potential therapeutic target. Research has demonstrated that MOTS-c levels decline with age, and supplementation with the peptide can help alleviate some age-associated metabolic dysfunctions [R].
MOTS-c and Insulin Sensitivity
In a study involving mice fed a high-fat diet, MOTS-c treatment prevented obesity and improved glucose homeostasis by enhancing insulin sensitivity and glucose utilization. In the same study, MOTS-c treatment restored insulin sensitivity in aged mice to levels comparable to those of young mice. MOTS-c may therefore be an effective therapeutic target for improving insulin sensitivity, particularly in the context of aging and age-related diseases [R].
MOTS-c has also been found to activate the Akt pathway in mouse skeletal muscle, leading to increased glucose uptake and improved insulin sensitivity. This is particularly significant, as skeletal muscle accounts for approximately 70% of insulin-stimulated glucose disposal [R].
MOTS-c and Osteoporosis
Recent research has highlighted the potential of MOTS-c, a mitochondrial-derived peptide, in combating osteoporosis. Studies have shown that MOTS-c plays a significant role in bone metabolism by promoting the proliferation, differentiation, and mineralization of osteoblasts, which are cells responsible for bone formation. Additionally, MOTS-c inhibits the formation and activity of osteoclasts, the cells that break down bone tissue. This dual action helps maintain a balance between bone formation and resorption. The peptide achieves these effects through various mechanisms, including the activation of the TGF-β/Smad signaling pathway, which is essential for the synthesis of type I collagen, a major component of the bone matrix [R, R, R].