As a result of the growing interest in mitochondrial-derived peptides, researchers are now enquiring about the best way to evaluate and handle MOTS-c for their experiments. MOTS-c is a short peptide that is generated from mitochondria, and it has been attracting the interest of researchers for any number of possible impacts, including the following:
- Weight-loss research
- Muscle cell proliferation studies
- Cell cycles, and anti-aging research
We include everything that researchers could need to know about this peptide in this MOTS-c guide. This includes referenced research studies and our suggestion on where to get research-grade MOTS-c online.
MOTS-c Peptide: What is it?
A peptide naturally produced and classed as a mitochondria-derived peptide (MDP) is called MOTS-c, which stands for mitochondrial open-reading-frame of the twelve S rRNA-C. It is composed of sixteen amino acids. Researchers have suggested that it may play a significant part in regulating metabolism and weight reduction and enhancing contractile force and phyiscal output as well as potential impacts on cell lifespan. First and foremost, mitochondria-derived peptides such as MOTS-c have been suggested to perform a “cytoprotective part in upkeeping mitochondrial function and cell viability under pressure.”
Not only is MOTS-c considered to be present in skeletal and muscular tissue, but it may also be present in several organs, including the liver and the brain. Additionally, research indicates that it may assist in regulating metabolic operations inside the organism, such as converting glucose into energy that can be utilized. By triggering the AMP-activated protein kinase (AMPK) pathway, MOTS-c has been hypothesized to make it possible for muscle cells to take in more glucose without causing a rise in insulin levels. AMPK is a metabolic regulator and a critical energy-detecting kinase activated when metabolic stress occurs.
The peptide is frequently suggested by research findings to possibly mimic the downstream action of physical exertion and muscle development on the organism. This may promote endogenous MOTS-c expression in skeletal muscle and circulation.
MOTS-c Peptide and Weight
Investigations purport that MOTS-c may be effective because it may target the skeletal muscle and improve glucose metabolism, both of which contribute to an increase in the organism’s use of energy. The biological impacts of the peptide may cause the folate cycle to be slowed down in the skeletal muscle, ultimately leading to the activation of AMPK.
According to research conducted in 2015 on mice with a diet rich in fat, MOTS-c seemed to have prevented diet-induced obesity. In addition, researchers have speculated that elevating AMPK levels might affect the expression of genes linked to inflammation, which normally leads to weight gain.
MOTS-c Peptide and Cell Lifespan
The investigation of MOTS-c has uncovered potential characteristics associated with the aging process. The m.1382A>C polymorphism, identified in the MOTS-c encoding mtDNA, was discovered by researchers in a study conducted in 2015. This polymorphism may be responsible for cell longevity and prolonged lifespan of the animal. In light of the findings of this investigation, the researchers put up the hypothesis that there is a “biological connection between MOTS-c and extended lifespan through the putative endocrine activity of this mitokine.”
MOTS-c Peptide and Insulin Resistance
Researchers have asserted that MOTS-c may play a significant role in enhancing insulin sensitivity. By serving as a regulator of metabolic homeostasis, it has been theorized that presentation with MOTS-c may counteract diet-induced and age-dependent muscle insulin resistance in mice.
The purpose of the investigation conducted in 2012 was to determine whether or not there was a connection between the levels of plasma MOTS-c and insulin sensitivity surrogates in animal research models either lean and undernourished, or obese. The researchers suggested that MOTS-c appeared to have had a favorable association with insulin sensitivity in the lean group. Still, this association was not detected in the obese models.
MOTS-c Peptide and Muscle Cells
Myostatin is considered to be the protein responsible for regulating the quantity of skeletal muscle mass present in the organism. Additionally, it may moderate the loss of skeletal muscle caused by insulin resistance.
Myostatin and plasma MOTS-c levels were indicated to have a potentially inverse connection in research conducted in 2021. By increasing AKT phosphorylation, the researchers speculated that MOTS-c may suppress the function of myostatin and other genes responsible for muscle atrophy. The researchers suggested that MOTS-c might be used as a possible approach for insulin resistance-induced skeletal muscular atrophy and the research of other disorders that cause muscle wasting.
MOTS-c Peptide and Bone Marrow
Research conducted in 2018 suggested that presentation with MOTS-c may potentially trigger the production of calcified nodules in the bone marrow stromal cells (BMSC) of rodents suffering from osteoporosis. Researchers speculated that the delivery of MOTS-c may have led to an increase in the expression of genes associated with the TGF-β/Smad pathway, which ultimately appeared to have resulted in osteogenic differentiation and an improvement in the cases of osteoporosis that were evaluated.
Another research that was conducted in 2016 aimed to determine whether or not MOTS c might prevent mice from developing osteoporosis after an ovariectomy. MOTS-c was given to the rats once daily for twelve weeks after removing the ovary. The researchers hypothesized that the presentation of MOTS-c may have significantly reduced bone loss in the research models.
Scientists interested in MOTS-c for sale are encouraged to navigate to the Core Peptides website for the highest-quality research compounds.
References
[i] Lee C, Kim KH, Cohen P. MOTS-c: A novel mitochondrial-derived peptide regulating muscle and fat metabolism. Free Radic Biol Med. 2016;100:182-187. doi:10.1016/j.freeradbiomed.2016.05.015
[ii] Yang Y, Gao H, Zhou H, Liu Q, Qi Z, Zhang Y, Zhang J. The role of mitochondria-derived peptides in cardiovascular disease: Recent updates. Biomed Pharmacother. 2019 Sep;117:109075. doi: 10.1016/j.biopha.2019.109075. Epub 2019 Jun 8. PMID: 31185388.
[iii] Lee C, Zeng J, Drew BG, Sallam T, Martin-Montalvo A, Wan J, Kim SJ, Mehta H, Hevener AL, de Cabo R, Cohen P. The mitochondrial-derived peptide MOTS[1]c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab. 2015 Mar 3;21(3):443-54. doi: 10.1016/j.cmet.2015.02.009. PMID: 25738459; PMCID: PMC4350682.
[iv] 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 Sep 4;28(3):516-524.e7. doi: 10.1016/j.cmet.2018.06.008. Epub 2018 Jul 5. PMID: 29983246; PMCID: PMC6185997.
[v] Reynolds JC, Lai RW, Woodhead JST, Joly JH, Mitchell CJ, Cameron-Smith D, Lu R, Cohen P, Graham NA, Benayoun BA, Merry TL, Lee C. MOTS[1]c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nat Commun. 2021 Jan 20;12(1):470. doi: 10.1038/s41467-020-20790-0. PMID: 33473109; PMCID: PMC7817689.
[vi] Elko Randrianarisoa, Angela Lehn-Stefan, Johannes Krier, Anja Böhm, Martin Heni, Martin Hrabě De Angelis, Andreas Fritsche, Hans-Ulrich Häring, Norbert Stefan, Harald Staiger, AMPK Subunits Harbor Largely Nonoverlapping Genetic Determinants for Body Fat Mass, Glucose Metabolism, and Cholesterol Metabolism, The Journal of Clinical Endocrinology & Metabolism, Volume 105, Issue 1, January 2020, Pages 14–25, https://doi.org/10.1210/clinem/dgz020
[vii] Fuku, Noriyuki & Pareja-Galeano, Helios & Zempo, Hirofumi & Alis, Rafael & Arai, Yasumichi & Lucia, Alejandro & Hirose, Nobuyoshi. (2015). The mitochondrial-derived peptide MOTS-c: A player in exceptional longevity?. Aging cell. 14. 10.1111/acel.12389.
[viii] Cataldo LR, Fernández-Verdejo R, Santos JL, et alPlasma MOTS-c levels are associated with insulin sensitivity in lean but not in obese individualsJournal of Investigative Medicine 2018;66:1019-1022.