MOTS-C 40MG vial

This product contains MOTS-C 40mg , with testing conforming the purity being 99.436%

FOR RESEARCH PURPOSES ONLY.

Preclinical Animal Research – MOTS-c (Mitochondrial-Derived Peptide)

High-Fat Diet Mouse Model (Metabolic Dysfunction / Obesity)

Study objective

Researchers investigated the metabolic effects of MOTS-c, a mitochondrial-derived peptide encoded within the 12S rRNA region of mitochondrial DNA, in diet-induced obese mice, focusing on insulin sensitivity, glucose metabolism, and energy homeostasis.

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Methods

Male mice were fed a high-fat diet (HFD) to induce obesity and insulin resistance. MOTS-c was administered via systemic injection during the treatment period.

Researchers assessed:

* Body weight and fat mass
* Glucose tolerance (GTT)
* Insulin sensitivity (ITT)
* Skeletal muscle glucose uptake
* Hepatic lipid accumulation
* Energy metabolism and substrate utilisation
* Gene expression related to metabolic regulation

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Results

Compared with untreated high-fat diet controls, MOTS-c administration produced significant metabolic improvements:

* Improved insulin sensitivity in peripheral tissues
* Enhanced glucose tolerance, with faster clearance of blood glucose during GTT
* Increased skeletal muscle glucose uptake, particularly in insulin-resistant states
* Reduction in diet-induced weight gain in treated groups
* Decreased hepatic lipid accumulation, indicating reduced fatty liver progression
* Improved metabolic flexibility, with increased utilisation of fatty acids and glucose depending on energy demand

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Key metabolic observation

One of the most notable findings was that MOTS-c appeared to act independently of major hormonal pathways, instead improving metabolism through cellular energy sensing and stress-response pathways rather than classical endocrine signalling.

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Exercise-Mimetic Mouse Studies (Physical Activity Response Model)

Study objective

To determine whether MOTS-c functions as an exercise-responsive mitochondrial signal, researchers evaluated its effects during metabolic stress and physical activity conditions.

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Methods

Mice were treated with MOTS-c under:

* Resting conditions
* High-fat diet conditions
* Acute exercise or exercise-mimicking metabolic stress

Researchers measured:

* Muscle endurance capacity
* Metabolic gene expression in skeletal muscle
* AMPK pathway activation
* Mitochondrial function markers
* Fat oxidation rates

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Results

MOTS-c administration produced an “exercise-like” metabolic signature:

* Activation of AMPK signalling pathways, a key cellular energy sensor
* Increased fatty acid oxidation in skeletal muscle
* Enhanced metabolic adaptation to energetic stress
* Improved exercise endurance capacity in treated animals
* Upregulation of genes associated with mitochondrial biogenesis and stress resistance
* Increased ability to maintain glucose homeostasis during metabolic stress

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Cellular Stress / Metabolic Challenge Models (In Vivo + Ex Vivo Integration)

Study objective

To examine MOTS-c’s role in cellular survival and adaptation under metabolic stress conditions.

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Methods

Animal and tissue-based experiments exposed cells and tissues to:

* Glucose restriction
* Oxidative stress conditions
* Metabolic overload environments

MOTS-c treatment was assessed for effects on:

* Cell survival pathways
* Mitochondrial function
* Stress-response gene expression
* Energy utilisation efficiency

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Results

MOTS-c demonstrated strong stress-adaptive effects:

* Increased cellular survival under metabolic stress conditions
* Enhanced mitochondrial efficiency and energy production balance
* Activation of adaptive nuclear gene expression programs linked to metabolism
* Improved resilience to metabolic overload and nutrient excess conditions

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Mechanistic preclinical findings

Across animal and integrated laboratory studies, MOTS-c has been shown to act through:

* Activation of AMPK (AMP-activated protein kinase) signalling
* Regulation of nuclear gene expression via mitochondrial-nuclear communication (“retrograde signalling”)
* Modulation of folate cycle and purine metabolism pathways (metabolic rewiring)
* Enhancement of cellular stress resistance mechanisms
* Improvement of insulin signalling efficiency in peripheral tissues

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Overall preclinical interpretation

In animal models, MOTS-c consistently demonstrates a profile of:

* Improved insulin sensitivity
* Enhanced glucose regulation
* Increased fat oxidation and metabolic flexibility
* Exercise-mimetic effects on skeletal muscle metabolism
* Protection against diet-induced metabolic dysfunction

Its effects are primarily driven by mitochondrial signalling to the nucleus, positioning it as a regulator of cellular energy adaptation rather than a classical hormone-like peptide.