MOTS-c

MOTS-c

$96.00

MOTS-c is a mitochondrial-derived peptide (MDP) consisting of 16 amino acids, encoded by the mitochondrial 12S rRNA gene. It has garnered significant attention in laboratory research for its role in regulating cellular metabolism, mitochondrial function, and energy homeostasis. Unlike traditional peptides derived from nuclear DNA, MOTS-c is encoded within the mitochondrial genome, making it a unique molecule of interest in studies involving metabolic stress and longevity.

In preclinical studies, MOTS-c has demonstrated the ability to modulate insulin sensitivity, glucose metabolism, and fatty acid oxidation under stress conditions. It has also shown promise in promoting mitochondrial biogenesis and maintaining cellular resilience during oxidative stress.

Researchers have been investigating MOTS-c in models exploring age-related metabolic dysfunctions, including obesity, type 2 diabetes, and exercise adaptation. Its mitochondrial origin opens up new avenues in the study of intracellular signaling and mitochondrial-nuclear cross-communication.

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Description

MOTS-c (Mitochondrial Open Reading Frame of the 12S rRNA type-c) is a naturally occurring mitochondrial-derived peptide (MDP) consisting of 16 amino acids. Encoded within the 12S rRNA region of mitochondrial DNA, MOTS-c represents a new frontier in metabolic and longevity research by demonstrating mitochondria’s ability to produce bioactive peptides with systemic regulatory effects.

Unlike traditional hormones or peptides synthesized from nuclear DNA, MOTS-c is unique in its mitochondrial origin. It translocates to the nucleus during metabolic stress and regulates gene expression associated with stress response, metabolism, and cellular protection. This makes it an important biomolecule in understanding mitochondrial-nuclear communication and systemic adaptation to environmental and physiological stress.

In vitro and in vivo studies suggest that MOTS-c plays a critical role in promoting insulin sensitivity and regulating glucose metabolism by activating the AMPK pathway, a master regulator of energy homeostasis. It has also been shown to enhance fatty acid oxidation and suppress oxidative stress pathways, which contributes to improved mitochondrial function and cellular health.

In experimental models involving high-fat diets and insulin resistance, administration of MOTS-c has been associated with improved metabolic profiles, reduced fat accumulation, and enhanced mitochondrial respiration. These findings make MOTS-c a valuable tool in metabolic disease research, including conditions such as obesity, type 2 diabetes, and age-associated metabolic decline.

Another area of interest involves MOTS-c’s effect on physical performance and muscle function. Preclinical data indicate that the peptide can increase exercise capacity and improve skeletal muscle mitochondrial activity. This has implications for aging research, where mitochondrial dysfunction contributes to sarcopenia, fatigue, and decreased resilience.

Furthermore, MOTS-c has shown potential in modulating inflammation and oxidative damage, particularly under metabolic stress or toxic insults. This positions it as a candidate for studies on cellular longevity, recovery from metabolic injury, and anti-aging interventions.

In aging models, MOTS-c administration has been correlated with improved metabolic stability, greater resistance to diet-induced obesity, and extended lifespan in mice, suggesting broader applications in age-related decline and mitochondrial therapeutics.

Research

MOTS-c has emerged as a groundbreaking mitochondrial-derived peptide (MDP) that challenges traditional views of mitochondrial function by demonstrating that mitochondria can encode and secrete regulatory peptides. Research on MOTS-c is rapidly expanding, primarily due to its significant role in metabolic adaptation, mitochondrial health, and aging.

Initial discoveries revealed that MOTS-c can translocate to the nucleus in response to metabolic stress, where it influences gene expression related to glucose metabolism, oxidative defense, and cellular energy regulation. This discovery marked a pivotal moment in mitochondrial biology, showing mitochondria as not just energy producers but also active regulators of cellular homeostasis.

Preclinical studies have shown that MOTS-c enhances glucose uptake in skeletal muscle and improves insulin sensitivity, making it highly relevant in research focused on metabolic disorders like type 2 diabetes. By activating AMPK and other signaling pathways, MOTS-c promotes mitochondrial biogenesis and enhances lipid oxidation, resulting in improved cellular resilience.

Animal models subjected to high-fat diets have exhibited improved metabolic health when administered MOTS-c, including reduced fat mass, increased lean muscle, and greater endurance. Notably, these effects occurred independently of food intake changes, suggesting a direct influence on energy regulation and mitochondrial efficiency.

In the field of aging, MOTS-c has gained attention for its potential to extend lifespan and delay the onset of age-associated metabolic dysfunction. Mouse models have demonstrated increased physical endurance, improved insulin sensitivity, and mitochondrial regeneration with MOTS-c treatment. These effects suggest its utility in research involving mitochondrial decline, chronic inflammation, and degenerative diseases.

Recent studies have also explored MOTS-c's influence on cognitive function and neurodegeneration. Given the critical role of mitochondria in neuronal survival and function, MOTS-c’s antioxidant and metabolic regulatory actions are being evaluated in models of Alzheimer's and Parkinson's diseases, although these areas require further exploration.

In summary, MOTS-c represents a promising molecule for scientific exploration in mitochondrial biology, metabolic disorders, and age-related decline. Its ability to modulate gene expression, activate protective signaling pathways, and support mitochondrial function places it at the forefront of current research in metabolic health and longevity.

For research purposes only. Not for human or veterinary consumption.

References:

  1. C. Lee, K. H. Kim, and P. Cohen, “MOTS-c: A novel mitochondrial-derived peptide regulating muscle and fat metabolism,” Free Radic. Biol. Med., vol. 100, pp. 182–187, Nov. 2016. [PMC]
  2. H. Lu et al., “MOTS-c peptide regulates adipose homeostasis to prevent ovariectomy-induced metabolic dysfunction,” J. Mol. Med. Berl. Ger., vol. 97, no. 4, pp. 473–485, Apr. 2019. [PubMed]
  3. K. H. Kim, J. M. Son, B. A. Benayoun, and C. Lee, “The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress,” Cell Metab., vol. 28, no. 3, pp. 516-524.e7, Sep. 2018. [PMC]
  4. S.-J. Kim et al., “The mitochondrial-derived peptide MOTS-c is a regulator of plasma metabolites and enhances insulin sensitivity,” Physiol. Rep., vol. 7, no. 13, p. e14171, Jul. 2019. [PubMed]
  5. R. Crescenzo, F. Bianco, A. Mazzoli, A. Giacco, G. Liverini, and S. Iossa, “A possible link between hepatic mitochondrial dysfunction and diet-induced insulin resistance,” Eur. J. Nutr., vol. 55, no. 1, pp. 1–6, Feb. 2016. [BMJ]
  6. L. R. Cataldo, R. Fernández-Verdejo, J. L. Santos, and J. E. Galgani, “Plasma MOTS-c levels are associated with insulin sensitivity in lean but not in obese individuals,” J. Investig. Med., vol. 66, no. 6, pp. 1019–1022, Aug. 2018. [PubMed]
  7. N. Che et al., “MOTS-c improves osteoporosis by promoting the synthesis of type I collagen in osteoblasts via TGF-β/SMAD signaling pathway,” Eur. Rev. Med. Pharmacol. Sci., vol. 23, no. 8, pp. 3183–3189, Apr. 2019. [PubMed]
  8. B.-T. Hu and W.-Z. Chen, “MOTS-c improves osteoporosis by promoting osteogenic differentiation of bone marrow mesenchymal stem cells via TGF-β/Smad pathway,” Eur. Rev. Med. Pharmacol. Sci., vol. 22, no. 21, pp. 7156–7163, Nov. 2018. [PubMed]
  9. N. Fuku et al., “The mitochondrial-derived peptide MOTS-c: A player in exceptional longevity?,” Aging Cell, vol. 14, Aug. 2015. [Research Gate]
  10. Q. Qin et al., “Downregulation of circulating MOTS-c levels in patients with coronary endothelial dysfunction,” Int. J. Cardiol., vol. 254, pp. 23–27, 01 2018. [PubMed]
  11. Y. Yang et al., “The role of mitochondria-derived peptides in cardiovascular disease: Recent updates,” Biomed. Pharmacother. Biomedecine Pharmacother., vol. 117, p. 109075, Jun. 2019. [PubMed]

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