MOTS-c(human) acetate
PRODUCTS SPECIFICATIONS
DESCRIPTION
Overview
| MDL | - |
|---|---|
| Molecular Weight | 2234.64 |
| Molecular Formula | C103H156N28O24S2 |
| SMILES | - |
Summary
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] .
IC50 & Target
|
AMPK |
GLUT4 |
AICAR |
In Vitro
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]
.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
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]
.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Appearance
Solid
Shipping
Room temperature in continental US; may vary elsewhere.
Storage
Sealed storage, away from moisture
| Powder | -80°C | 2 years |
|---|---|---|
| -20°C | 1 year |
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Solvent & Solubility
DMSO : 4 mg/mL ( 1.79 mM ; Need ultrasonic)
Stock Solutions
| Concentration Solvent Mass | 1 mg | 5 mg | 10 mg |
|---|
| 1 mM | 0.4475 mL | 2.2375 mL | 4.4750 mL |
| 5 mM | --- | --- | --- |
| 10 mM | --- | --- | --- |