Mots-c

Mots-c

Mots-c peptide is a short peptide encoded in the mitochondrial genome and a member of the larger group of mitochondrial-derived peptides (MDPs). MDPs have recently been found to be bioactive hormones that play important roles in mitochondrial communication and energy regulation. Originally thought to be related to the mitochondria only, new research has revealed that many MDPs are active in the cell nucleus and that some even make their way into the blood stream to have systemic effects. MOTS-c is a newly identified MDP that has, to date, been found to play important roles in metabolism, weight regulation, exercise capacity, longevity, and even processes leading to disease states like osteoporosis. MOTS-c has been found in the nucleus of cells as well as in the general circulation, making it a bonafide natural hormone. The peptide has been targeted for intensive research in the last five years due to its therapeutic potential.

Mots-c Peptide Review

 

MOTS-C Structure, De BQUB17-JHolguera – Trabajo propio, CC BY-SA 4.0
Source: Wikipedia

Sequence: Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Arg
Molecular Formula: C₁₀₁H₁₅₂N₂₈O₂₂S₂
Molecular Weight: 2174.64 g/mol
PubChem SID: 255386757
CAS Number: 1627580-64-6
Synonyms: Mitochondrial open reading frame of the 12S rRNA-c, MT-RNR1

Mots-c

 Mots c Peptide Muscle Metabolism

Research in mice indicates the MOTS-c can reverse age-dependent insulin resistance in muscles, thereby improving muscle uptake of glucose. It does this by improving skeletal muscle response to AMPK activation, which in turn increases the expression of glucose transporters. It is important to note that this activation is independent of the insulin pathway and thus offers an alternative means of boosting glucose uptake by muscles when insulin is ineffective or in insufficient quantity. The net result is improved muscle function, enhanced muscle growth, and decreased functional insulin resistance.

Mots-c Peptide Metabolism

Research in mice has shown that low levels of estrogen lead to increased fat mass and dysfunction of normal adipose tissue. This scenario increases the risk of developing insulin resistance and, subsequently, the risk of developing diabetes. Supplementing mice with MOTS-c, however, increases brown fat function and reduces the accumulation of adipose tissue. It also appears that the peptide prevents adipose dysfunction and the adipose inflammation that typically precedes insulin resistance.

It appears that at least part of the influence that MOTS-c has on fat metabolism is mediated through activation of the AMPK pathway. This well-defined pathway is turned on when cellular energy levels are low and it drives the uptake of both glucose and fatty acids by cells for metabolism. It is also the pathway that is activated in ketogenic diets, like the Atkin’s diet, which promote fat metabolism while protecting lean body mass. MOTS-c targets the methionine-folate cycle, increases AICAR levels, and activates AMPK.

New research suggests that MOTS-c can actually leave the mitochondria and make its way to the nucleus where the peptide can affect nuclear gene expression. Following metabolic stress, MOTS-c has been shown to regulate nuclear genes involved in glucose restriction and antioxidant responses

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