MOTS-C Peptide Vial Belgium
Direct Sarms does not encourage or promote the use of any of these products in a personal capacity (i.e. human consumption), nor are the products intended to be used as a drug, stimulant or for use in any food products.
A number of scientific advances recently made in high-resolution sequencing have resulted in the discovery of peptides derived from the mitochondrial genome. Among these peptides is 12S tRNA-c which encodes a 16-amino acid named MOTS-c, as well as six small human-like peptides named SHLP1-6. Research has suggested that these may aid treatments for a number of conditions.
Clinic trials have evidenced one of these benefits appears to be that it regulates insulin sensitivity and metabolic homeostasis, allowing it to reduce insulin resistance  and decrease obesity. Research suggests that its primary target organ is the skeletal muscle and metabolic regulation is achieved via the folate-purine-AMPK pathway.
During trials of MOTS-c treatment on mice  it was discovered that in these mice, both age-dependent and high-fat-diet-induced insulin resistance was prevented. The research also showed a reduction in diet-induced obesity, which may have implications for the treatment or prevention of obesity-related conditions. It is therefore hypothesised that the mitochondria MOTS-c is derived from could actively regulate metabolic homeostasis at the cellular and organismal level through the peptides their genome encodes.
While the possibility of using MOTS-c to form treatments for insulin resistance and obesity in many sectors of the population, some research has looked particularly at the implications for the post-menopausal state. This state is a particularly risky time for metabolic disorders which include weight gain and reduced energy expenditure. These can lead to an increased risk of cancer and cardiovascular diseases.
Clinical trials on mice showed that low levels of estrogen after ovariectomy resulted in an increased fat mass overload and insulin resistance developed due to the disturbance of normal adipose function. Following treatment with MOTS-c, the research showed that brown fat activation increased, while both OVX-induced fat accumulation and inflammatory invasion in white adipose tissue was reduced. Additionally, a blocker of the AMPK  pathway was found to reduce the effect of MOTS-c in regulating adipocyte lipid metabolism, while a MOTS-c activated AMPK pathway improved both energy dissipation and insulin sensitivity.
The implication of these trials would suggest that MOTS-c peptide has the potential to be used to develop treatments of menopausal induced metabolic dysfunction. Furthermore, the research suggests that it may play a role in the treatment and prevention of diabetes and obesity-related diseases across the population.
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