MOTS-c Peptide: Insulin, glucose, mitochondria and more

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The 12S rRNA area of the mitochondrial genome encodes MOTS-c, a peptide produced from mitochondria, which consists of 16 residues. This indicates that an mRNA strip was not processed from the genetic information translated into the peptide’s amino acid sequence.

The compound is translated from a link of rRNA, whose primary function is considered to aid ribosomes in digesting genetic information rather than carrying it. Since its discovery in 2015, MOTS-c has garnered interest due to its possible function in metabolic control and age-related diseases.

Numerous studies have suggested that MOTS-c may potentially influence insulin sensitivity, mitochondrial function, cellular metabolism, and physiological aging on a cellular level. There is data from studies indicating that MOTS-c might:

  • Raise the efficiency of glucose absorption and use
  • Increase organism responsiveness to insulin
  • Initiate the process of mitochondrial biogenesis
  • Defend against oxidative stress.

Research indicates that these actions may have possible ramifications for the context of diabetes, obesity, and age-related illnesses, as they may enhance metabolic and cellular functions.

MOTS-c Peptide: Mechanism of Action

Kim et al (2018) suggested that MOTS-c may reach the nucleus during metabolic stress. Through this translocation, MOTS-c has been hypothesised to regulate the expression of adaptive genes inside the nucleus.

Because of its release into the circulation, MOTS-c is sometimes called a “mitochondriahormone” or a “mitokine”. Among mitochondrial-derived peptides (MDPs), MOTS-c has received greater attention than Humanin and other, similar research compounds. Despite Humanin's receptor-binding versatility, no MOTS-c-specific receptors have been discovered.

The folate cycle plays a role in MOTS-c circulation regulation, and cell aging appears to affect its expression. Research indicates that endogenous levels of this peptide may often decrease over time.

MOTS-c is translocated from mitochondria to the nucleus in response to stress. Investigations purport that in this way, MOTS-c may control the levels of two crucial regulators of energy balance: Activated protein kinase (AMPK) and 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR).

In general, MOTS-c is believed to be an important modulator of metabolic processes. Metabolic diseases like obesity and insulin resistance after menopause may be amenable to its impact in this form. Research has indicated that it may have anti-aging effects via specific cellular pathways associated with aging, and it may also exhibit cardiometabolic potential due to its proposed involvement in maintaining the balance of energy inside cells.

More investigation is required to analyse the complex pathways by which MOTS-c may regulate cellular metabolism and its possible impact on physiological and pathological states.

MOTS-c Peptide Potential

MOTS-c has suggested encouraging results in preclinical investigations, which might lead to several downstream impacts upon the organism. Some of the possible properties of MOTS-c, based on current results, may be as outline below, even though an additional study is necessary to comprehend its research applications completely:

MOTS-c Peptide and Metabolism: Hormonal shifts in aging research models, particularly in female species, may induce metabolic dysfunction, increasing the risk of diseases, including obesity and insulin resistance. Lu et al (2019) examined the impact of MOTS-c on these metabolic alterations in ovariectomy-stricken mice.

According to research, ovariectomy is considered to cause insulin resistance through an impact on fat mass and adipose tissue function. On the other hand, obesity and insulin resistance are hypothesised to be averted by MOTS-c. These results suggest that MOTS-c may potentially support research models’ metabolisms return to normal and reverse the onset of obesity and insulin resistance.

MOTS-c Peptide and Obesity: Lee et al (2015) examined how MOTS-c may affect weight control in a mouse model. Presenting mice with MOTS-c daily combined with a high-fat meal appeared to have resulted in substantial weight loss compared to presenting mice with a standard diet alone. In the latter, no discernible weight loss occurred.

These results suggest that MOTS-c might have an impact in weight regulation. Nevertheless, further research is needed to properly understand the precise processes by which MOTS-c may affect weight loss when combined with a high-fat diet. It is important to note that results of these studies on animals in the laboratory do not apply to humans in any way.

MOTS-c Peptide and Cell Aging: Over time, the organism's capacity to react to metabolic stress diminishes, and biological processes progressively decline. By improving physical ability and mitochondrial function, this process, called senescence, may be reduced.

Aged animal models exhibited lower MOTS-c levels than their younger counterparts, dropping about 21 percent. NAD+, considered to be an important regulator of cellular signalling and survival pathways, is one of the age-related modifiers with which MOTS-c is suggested to share metabolic pathways.

Reynolds et al (2021) researched mice and suggested that the daily exposure of MOTS-c for two weeks may have increased physical performance and decreased age-related reductions in various age groups of the animal models examined.

An abnormal build-up of calcium phosphate crystals in artery walls is described as vascular calcification (VC), a consequence of atherosclerosis and chronic renal disease. It has been reported that MOTS-c may monitor cardiovascular function for this condition. Results reported that MOTS-c may successfully avoid vascular calcification in an animal investigation into its relevance in the context of VC research.

Researchers hypothesised that the peptide’s positive impact may have been due to its activation of AMPK signalling. However, the research significance of these results in research models needs additional exploration.

MOTS-c Peptide and Muscle: Mitochondria are essential for the proper functioning of skeletal muscles and for transmitting signals to other organs caused by physical activity. Physical strain and MOTS-c appear to work together to enhance the expression of the PGC-1α gene, a gene involved in energy metabolism and mitochondrial biogenesis.

After MOTS-c presentation in mice, cellular levels of GLUT4 and AICAR, two AMPK agonists, were hypothesised to have increased, suggesting that this compound may activate skeletal muscle AMPK, a regulator of physical activity response. According to research by Li et al (2022), the combined effects of MOTS-c and physical activity on 24 genes involved in angiogenesis, inflammation, and apoptosis seemed to modify pathogenic genes.

Scientists interested in high-quality, affordable MOTS-c are encouraged to click here.

Disclaimer: Please note that none of the substances mentioned in this article have been approved for human or animal consumption. Unlicensed individuals should only acquire or utilise peptides in strictly contained research environments such as laboratories.