MOTS-c(human) acetate 

MOTS-c(human) acetate is a mitochondrial-derived peptide. MOTS-c(human) acetate induces the accumulation of AMP analog AICAR, increases activation of AMPK and expression of its downstream GLUT4. MOTS-c(human) acetate induces glucose uptake and improves insulin sensitivity. MOTS-c(human) acetate has implications in the regulation of obesity, diabetes, exercise, and longevity^[1].

MOTS-c inhibits the folate cycle at the level of 5Me-THF, resulting in an accumulation of AICAR [5-aminoimidazole-4-carboxamide ribonucleotide). MOTS-c also increases cellular NAD⁺ levels, which are also nucleotide precursors^[1].
MOTS-c is a mitochondrial signal that stimulates cellular glucose uptake while suppressing respiration. The glucose taken up in response to MOTS-c is routed to the anabolic pentose phosphate pathway (PPP), which provides carbon sources for the synthesis of purines, rather than being metabolized through glycolysis. In addition, MOTS-c increases the levels of carnitine shuttles, which transport activated fatty acids into the mitochon-dria for β-oxidation, increases the level of a β-oxidation intermediate, and reduces intracellular levels of essential and non-essential fatty acids, suggesting enhanced lipid utilization; myocytes that stably overexpress MOTS-c also exhibits increased glucose uptake^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

MOTS-c injections in mice show activation of skeletal muscle AMPK and increased the level of its downstream glucose transporter GLUT4. MOTS-c may also act as a potential mitochondrial signal that mediates an exercise-induced mitohormesis response, thereby stimulating physiological adaptation and increased tolerance to exercise^[1].
The primary target organ of MOTS-c appears to be skeletal muscle and fat. MOTS-c levels in mice decline with age in skeletal muscle and in circulation concomitantly with the age-dependent development of insulin resistance. Restoring MOTS-c levels by systemic injections in older mice (12 mo.) successfully reverses age-dependent skeletal muscle insulin resistance^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

2234.64

C₁₀₃H₁₅₆N₂₈O₂₄S₂

Solid

White to off-white

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

MRWQEMGYIFYPRKLR

Room temperature in continental US; may vary elsewhere.

Sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

• [1]. Changhan Lee, et al. MOTS-c: A Novel Mitochondrial-Derived Peptide Regulating Muscle and Fat Metabolism. Free Radic Biol Med. 2016 Nov;100:182-187.  [Content Brief]