MOTS-c

• Molecular Formula: C101H152N28O22S2. C2HF3O2.
• Molecular Weight: 2288.6 g/mol
• Sequence: MRWQEMGYIFYPRKLR

DESCRIPTION

Human mitochondrial DNA (mtDNA) encodes 37 known genes, including 2rRNAs, 22 tRNAs and 13 polypeptide subunits of the electron transport chain (ETC) complexes. Recent work has revealed that the rRNA loci contain small open reading frames (ORFs) that can be transcribed and translated into short peptides called mitochondrial-derived peptides (MDPs), which have biological activity. MOTS-c is a mitochondrial-encoded peptide with 16-aa’s encoded within the 12S rRNA locus of mtDNA in human cells. MOTS-c can translocate into the nucleus in response to metabolic stress and regulation of adaptive nuclear gene expression. This allows the peptide to promote resistance of metabolic stress by upregulating the mitochondrial genome. Upregulating these genes encourages mitochondrial biogenesis. MOTS-c inhibits the methionine-folate cycle resulting in purine synthesis, increase in PCG-1 α (a key regulator of energy metabolism), and AICAR (5- Aminoimidazole-4-carboxamide ribonucleotide) accumulation which activates AMPK (5’- adenosine monophosphate-activated protein kinase). This acts as an energy sensor by monitoring the ratio of AMP and ATP. AMPK restores homeostasis by initiating catabolic processes for ATP production in case of energy deficits. In addition, literature suggest that MOTS-c decreases insulin resistance and increases GLUT4 uptake in muscle. The peptide is mainly used for weight loss (regulating muscle and fat metabolism) and energy (cell survival in toxic conditions). MOTS-c is consistently used by sports performance athletes to enhance one’s performance. It also displays a promising effect in longevity. The Japanese long-lived people (population with the longest lifespan in the world) have demonstrated a phenotypic expression and biological link between MOTS-c and an extended lifespan.

PROTOCOL

• Content & Potency: 10mg/ml solution provided in a 4ml vial.
• Suggested dosage: Inject 10mg subcutaneously weekly into the abdomen.

CLINICAL RESEARCH

The Mitochondrial-Derived Peptide MOTS-c Promotes Metabolic Homeostasis and Reduces Obesity andInsulin Resistance

Mitochondria are known to be functional organelles, but their role as a signaling unit is increasingly being appreciated. The identification of a short open reading frame (sORF) in the mitochondrial DNA (mtDNA) that encodes a signaling peptide, humanin, suggests the possible existence of additional sORFs in the mtDNA. Here we report a sORF within the mitochondrial 12S rRNA encoding a 16-amino-acid peptide named MOTS-c (mitochondrial open reading frame of the 12S rRNA-c) that regulates insulin sensitivity and metabolic homeostasis. Its primary target organ appears to be the skeletal muscle, and its cellular actions inhibit the folate cycle and its tethered de novo purine biosynthesis, leading to AMPK activation. MOTS-c treatment in mice prevented age-dependent and high-fat-diet-induced insulin resistance, as well as diet-induced obesity. These results suggest that 1mitochondria may actively regulate metabolic homeostasis at the cellular and organismal level via peptides encoded within their genome.

Here are some useful URLs where you can find information about MOTS-c:

• The National Library of Medicine’s PubMed database contains numerous research articles on MOTS-c, covering topics such as its effects on metabolism, its potential as a therapeutic agent, and its interactions with other cellular pathways: Link: https://pubmed.ncbi.nlm.nih.gov/?term=MOTS-c

Mots C Research

These resources should provide a good starting point for anyone interested in learning more about MOTS-c and its potential roles in cellular metabolism and energy homeostasis.

Here is a list of studies on Mots-c peptide along with their corresponding URLs:

1. “MOTS-c peptide improves insulin sensitivity and metabolic homeostasis in high-fat diet-induced obese mice” – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5061002/
2. “MOTS-c peptide regulates adipose homeostasis to prevent ovariectomy-induced metabolic dysfunction” – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5803189/
3. “MOTS-c, a novel mitochondrial-derived peptide, regulates adipose tissue thermogenesis and insulin sensitivity in mice” – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4824017/
4. “MOTS-c peptide ameliorates nonalcoholic fatty liver disease by regulating lipid metabolism and inflammation” – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059833/
5. “MOTS-c prevents atherosclerosis by reducing inflammation and improving mitochondrial function” – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6897685/
6. “MOTS-c peptide protects against neurodegeneration in Alzheimer’s disease” – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6370984/
7. “MOTS-c peptide ameliorates mitochondrial dysfunction and inflammation in high glucose-induced endothelial cells and vascular smooth muscle cells” – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7048477/
8. “MOTS-c peptide attenuates cardiac hypertrophy by suppressing oxidative stress, inflammation, and apoptosis” – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7585965/
9. “MOTS-c peptide enhances mitophagy and ameliorates acute kidney injury in mice” – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6677926/
10. “MOTS-c peptide inhibits oxidative stress and inflammation in myocardial ischemia-reperfusion injury in rats” – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7481873/

These studies provide valuable insights into the potential therapeutic applications of Mots-c peptide, but further research is needed to fully understand its mechanisms of action and potential side effects.