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MOTS-c(human) acetate

CAS No. :

MCE 站：MOTS-c(human) acetate

产品活性：MOTS-c(human) acetate 是一种线粒体衍生的肽，可诱导 AMP 类似物 AICAR 的积累，增加 AMPK 的激活及其下游 GLUT4 的表达。MOTS-c(human) acetate 可诱导葡萄糖摄取并改善胰岛素敏感性，对肥胖，糖尿病，运动和长寿的调节具有影响。

研究领域：Epigenetics  |  PI3K/Akt/mTOR  |  Membrane Transporter/Ion Channel

作用靶点：AMPK  |  GLUT

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.
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.

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.
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.

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