Intermediate Peptide Mots-C (human) for Osteoporosis CAS 1627580-64-6

What is Peptide Intermediate Mots-C (human) For Osteoporosis CAS 1627580-64-6?

Mitochondria are known to be functional organelles, but their role as a signaling unit is increasingly being appreciated. The identification of a short open reading frame (SORF) in the mitochondrial DNA (mtDNA) that encodes a signaling peptide, humanin, suggests the possible existence of additionalSORFS in the mtDNA. Here we report a SORF within the mitochondrial 12S RRNA encoding a 16-amino-acid peptide named MOTS-C (mitochondrial open reading frame of the 12S RRNA-C) 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.

These results suggest that mitochondria may actively regulate metabolic homeostasis at the cellular and organismal level via peptides encoded within their genome.

Application:

MOTS-C in Osteoporosis

Osteoporosis is a multi-factor and age-related metabolic disease. Bone mesenchymal stem cells (BMSCS) are the progenitor cells of osteoblasts and adipocytes and play an essential role in the process of bone formation.

AMPK can stimulate the proliferation, differentiation and mineralization of osteoblasts, which exerts an important role in the cellular functions of osteoblasts. Osteoblasts are cells that make bone. Bone mass is maintained by a balance between the activity of osteoblasts that form bone and other cells called osteoclasts that break it down.

Studies show that BMSC’s treated with MOTS-C upregulated expression levels of ALP, Bglap, and Runx2. This resulted in the formation of mineralized nodules, indicating the osteogenic capacity of BMSC’s regulated by MOTS-C. In simple nonscientific terms,

MOTS-C promotes cell differentiation of BMSCs to osteoblasts = bone formation.

Function:

Promotes fatty acid metabolism in the liver

Promotes metabolic flexibility and homeostasis

Helps regulate mitochondrial energy

Protects against age and diet dependent insulin resistance and obesity

Helps with weight loss

Promotes resistance to metabolic stress

Improves exercise capacity

Helps prevent osteoporosis

Improves glucose regulation

Promotes cell differentiation to form osteoblasts

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