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MOTS-c is a novel mitochondrial-derived peptide from the mitochondrial protein that is responsible for the synthesis of ATP. It also has been shown to significantly increase insulin sensitivity and can decrease the amount of glucose that is broken down by adipose cells. It has also been shown to reduce fatty liver disease, and there have also been numerous studies to show how effective this peptide is in possibly aiding with diabetes This specific peptide has shown to be able to promote a positive shift in insulin sensitivity, where exercise and diet can lead to muscles regaining their normal function. This decreases the levels of insulin and leptin resistance .
Additionally, it has been found that levels of insulin resistance and glucose tolerance are significantly reduced. More importantly, studies have shown that MOTS-C has the ability to improve the function of the beta islet cells, which are responsible for the production of insulin. This presents a potential mechanism for the treatment of Type 2 Diabetes. Another study examined the effects of MOTS-C on lean mass, body fat mass, and fat-free mass. It was concluded that MOTS-C significantly increased lean mass and did not have any negative effects on fat mass or fat-free mass . In short, MOTS-C is a peptide that can be used to treat diabetes and Alzheimer’s, significantly improve insulin sensitivity, and reduce body fat levels in animal models.
MOTS-c is a 16 amino acid peptide that regulates insulin sensitivity and metabolic homeostasis. Its primary target organ appears to be the skeletal muscle and its cellular actions inhibit the folate cycle and its tethered de novo purine biosynthesis, leading to AMPK activation. MOTS-c treatment in mice prevented age-dependent and high-fat diet-induced insulin resistance, as well as diet-induced obesity. MOTS-c is a mitochondrial peptide with diverse biological activities.1,2,3
It increases osteogenic differentiation and the formation of calcified nodules in rat bone mesenchymal stem cells (BMSCs) when used at a concentration of 1 µM.1 MOTS-c decreases 5-methyl-tetrahydrofolate levels, blocking de novo purine biosynthesis, increases accumulation of 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), and activates AMPK in HEK293 cells.2 It increases glycolysis in HEK293 cells in an AMPK-dependent manner. In vivo, MOTS-c (0.5 mg/kg per day, i.p.) increases glucose clearance in mice fed a normal diet. It increases skeletal muscle AMPK activation and GLUT4 expression, as well as prevents high-fat diet-induced obesity and hyperinsulinemia in CD-1 mice. MOTS-c (5 mg/kg) increases AMPK activation, reduces protein levels of the angiotensin II type 1 (AT1) and endothelin B (ETB) receptors and left ventricular posterior wall thickness, and attenuates aortic calcification in a rat model of secondary myocardial remodeling.3
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For more information on MOTS-c peptide please visit Pubmed.
References & Product Citations
Product Description References
1. Hu, B.-
2. Lee, C., Drew, B.G., Sallam, T., et al. The mitochondrial-
3. Wei, M., Gan, L., Liu, Z., et al. Mitochondrial-
Mitochondrial open reading frame of the 12S rRNA-c
Lyophilized mots-c peptide is stable at room temperature for 90 days. However, it should be stored in a freezer below -8C for any extended period of time
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Products on the website are not intended for use in the diagnosis, cure, mitigation, treatment, or prevention of disease and are not intended to affect the structure or any function of the body. The use of our products are for only research/laboratory purposes.
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