MOTS-C

Chemical Makeup:

• Molecular Formula: C101, H152, N28, O22, S2
• Molecular Weight: 2174.6 g/mol
• Synonyms: Mitochondrial Open Reading Frame of the 12S rRNA-c, HN13, 12S rRNA-c peptide.

Sequence:

• Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Arg

[MOTS-c] and Metabolic Homeostasis

Studies in murine models suggest that [MOTS-c] plays a significant role in the regulation of whole-body metabolism. In high-fat diet (HFD) induced obesity models, administration of the peptide was observed to suppress weight gain and improve insulin sensitivity. The peptide appears to promote the browning of white adipose tissue and enhance thermogenesis, thereby increasing energy expenditure. Research by Lee et al. (2015) indicates that [MOTS-c] targets skeletal muscle to improve glucose clearance, potentially offering a pathway to mitigate diet-induced insulin resistance.

[MOTS-c] and Physical Performance

[MOTS-c] has been characterized in academic literature as an "exercise mimetic." In aged mouse models, treatment with the peptide was shown to enhance physical capacity, including improved running time and grip strength. It is hypothesized that [MOTS-c] levels naturally rise in skeletal muscle and circulation during physical exertion. Exogenous application in research settings suggests a potential restoration of physical performance parameters that typically decline with age, likely through the enhancement of skeletal muscle cellular metabolism.

[MOTS-c] and Bone Health

Emerging research links mitochondrial function to skeletal integrity. Studies involving ovariectomized murine models (a standard model for post-menopausal osteoporosis) indicate that [MOTS-c] may preserve bone mass. Mechanisms identified include the promotion of osteoblast differentiation (bone formation) and the potential inhibition of osteoclast activity (bone resorption). Specifically, the peptide has been observed to influence the TGF- b/Smad signaling pathway, which is critical for mesenchymal stem cell differentiation into osteoblasts.

[MOTS-c] and Longevity

The role of [MOTS-c] in aging is a subject of ongoing investigation. It has been observed that endogenous levels of [MOTS-c] decline with age in humans. In preclinical longevity studies, intermittent administration of the peptide to middle-aged mice was associated with an extended healthspan and lifespan. This effect is believed to be mediated through the optimization of mitochondrial metabolic flexibility and the reduction of age-associated accumulation of senescent markers.

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Side Effects:

 In animal research studies, [MOTS-c] has generally been well-tolerated. However, injection site reactions (redness or irritation) have been noted in some murine models. Because [MOTS-c] strongly influences glucose metabolism, there is a theoretical risk of hypoglycemia if metabolic variables are not controlled, although this has primarily been observed in conjunction with other metabolic interventions. Long-term toxicity profiles in non-human primates or humans have not been established.

Disclaimer: 

RESEARCH USE ONLY. This product is intended only for in vitro and laboratory research purposes. It is not for human or animal consumption, therapeutic use, or diagnostic procedures.