MOTS-c 5mg

MOTS-c 5mg, short for Mitochondrial ORF of the 12S rRNA Type-C, is a 16-amino acid peptide originating from the mitochondrial genome's 12S rRNA region. Mitochondrial-derived peptides (MDPs) exhibit a diverse array of physiological functions.⁽¹⁾

Studies involving mice revealed that MOTS-c has a significant impact on inflammatory responses. Experimental setups included the measurement of pro-inflammatory and anti-inflammatory factors in the serum of mice after MOTS-c treatment. Results indicated a notable reduction in pro-inflammatory factors and an increase in anti-inflammatory factors upon MOTS-c administration. Additionally, the peptide exhibited an ability to reduce pain in mice, as evidenced by decreased licking time in the formalin test. The analgesic and anti-inflammatory effects were associated with the activation of the AMPK pathway and inhibition of the MAP kinase/c-Fos pathway, as demonstrated by changes in phosphorylation levels and gene expression. Overall, these findings highlight MOTS-c's potential in modulating inflammatory processes in animal models.^(2-4)

MOTS-c's role in regulating metabolic conditions like obesity and diabetes was explored in various studies. These investigations typically involved assessing MOTS-c levels in relation to metabolic parameters such as insulin sensitivity, glucose utilization, and body weight. Results consistently showed associations between MOTS-c levels and improved metabolic outcomes, including enhanced insulin sensitivity, glucose balance, and prevention of weight gain.⁽⁵⁾Additionally, MOTS-c was implicated in promoting glucose utilization, inhibiting oxidative stress, and protecting against endothelial dysfunction, highlighting its potential therapeutic value in addressing metabolic disorders and related complications.⁽⁶⁾ Moreover, studies suggested a link between MOTS-c and longevity, with findings indicating that higher MOTS-c levels may be beneficial in delaying aging-related metabolic decline and associated diseases.⁽¹⁾

MOTS-c's involvement in mitochondrial signal transduction pathways was investigated in cellular and animal models. Experimental setups included examining the effects of MOTS-c on mitochondrial gene expression, AMPK activation, and cellular stress responses. Results revealed that MOTS-c can improve mitochondrial function, enhance stress resistance, and regulate nuclear gene expression by interacting with transcription factors.⁽⁷⁾ The peptide's ability to modulate cellular responses to metabolic stress underscores its potential as a therapeutic agent for age-related diseases and metabolic disorders. Moreover, studies suggested that MOTS-c may exert protective effects against cardiovascular diseases by improving heart structure and function, promoting angiogenesis, and reducing inflammation, highlighting its multifaceted roles in maintaining cardiovascular health.⁽⁸⁾

References: 1. Zheng Y, Wei Z, Wang T. MOTS-c: A promising mitochondrial-derived peptide for therapeutic exploitation. Front Endocrinol (Lausanne). 2023;14:1120533. 2. Lee C, Zeng J, Drew BG, et al. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab. 2015;21(3):443-454. 3. Yin X, Jing Y, Chen Q, Abbas AB, Hu J, Xu H. The intraperitoneal administration of MOTS-c produces antinociceptive and anti-inflammatory effects through the activation of AMPK pathway in the mouse formalin test. Eur J Pharmacol. 2020;870:172909. 4. Yang B, Yu Q, Chang B, et al. MOTS-c interacts synergistically with exercise intervention to regulate PGC-1α expression, attenuate insulin resistance and enhance glucose metabolism in mice via AMPK signaling pathway. Biochim Biophys Acta Mol Basis Dis. 2021;1867(6):166126. 5. Lee C, Zeng J, Drew BG, et al. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab. 2015;21(3):443-454. 6. Yang B, Yu Q, Chang B, et al. MOTS-c interacts synergistically with exercise intervention to regulate PGC-1α expression, attenuate insulin resistance and enhance glucose metabolism in mice via AMPK signaling pathway. Biochim Biophys Acta Mol Basis Dis. 2021;1867(6):166126. 7. Kim KH, Son JM, Benayoun BA, Lee C. The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress. Cell Metab. 2018;28(3):516-524.e7. 8. Yuan J, Wang M, Pan Y, et al. The mitochondrial signaling peptide MOTS-c improves myocardial performance during exercise training in rats. Sci Rep. 2021;11(1):20077.