Follistatin-344: A Potential Activin-binding Protein and Myostatin Inhibitor

Follistatin is a glycoprotein generated and produced in the liver but also in other body tissues.

The peptide’s primary function is to deactivate TGF-beta superfamily proteins. It can help reduce the effects of avidin, myostatin, and FSH (follicle-stimulating hormone).

The Potential Effects Of Follistatin On Muscle Growth

Growth differentiation factor-8 is myostatin. It’s a myokine that myocytes produce and release to stop muscle growth. It belongs to the TGF-beta family and is Follistatin-sensitive.

According to research, myostatin-deficient animals have considerable muscle mass. As a result, scientists believe administering Follistatin can help with muscle growth and treat muscular dystrophy.

The peptide increases lean muscle mass in mice without requiring them to exercise or eat particular diets, implying that gains could be high when combined with the appropriate training or diet.

Peptide delivery through gene therapy may provide long-term advantages for muscular dystrophy patients. Follistatin gene therapy has enhanced muscle mass and strength in typical and dystrophic mice for more than two years in mouse models.

Research shows it can boost muscle growth by enhancing the insulin/IGF-1 pathway. Follistatin, in particular, suppresses IGF-1 expression in the muscles. The peptide has been linked to insulin signaling because it can cause the pancreas to release more insulin.

Follistatin and Cancer

Follistatin is over-expressed in a small percentage of breast cancer cases but under-expressed in the majority. It inhibits epithelial cell migration produced by avidin in mice models, but it is absent in breast cancers in the general population. Follistatin is involved in benign proliferative breast diseases.

According to studies, bone morphogenic protein (BMP) may be a causal agent in altering normal esophageal tissue to Barrett’s esophagus, a cancer precursor.

The Effects Of Follistatin On Cell Proliferation

According to breast cancer research, the peptide stimulates cell proliferation while inhibiting metastasis. In most tissues, this is a proven pattern. The compound expression is necessary primarily in proliferating hepatocytes.

In rat models, Follistatin-mediated inactivation of avidin is required for proliferation. This mediation could explain why Follistatin is linked to increased tumor development but decreased tumor invasion and metastasis.

The Role Of Follistatin In Congenital Blindness

Fusing the optic nerve during fetal development is essential for human vision. Studies show increased TGF-beta protein levels cause optic nerve fusion following blindness.

Follistatin’s inhibitory impact could override these proteins’ functions and lead to fusion, ensuring that the optic nerve remains intact after blindness is alleviated.

The effects of Follistatin supplementation during developing periods of pregnancy to ensure optic nerve fusion are being studied.

Insulin Deficiency And Diabetes

Over-expression of Follistatin in mouse models increases the mass of beta cells in the islets of Langerhans, which are responsible for insulin synthesis. This process can result in an increase in insulin levels, a decrease in excess glucose levels, and a relief of diabetes symptoms.

Scientists expect that using the peptide in treating diabetes will shed some information on how to approach and improve type 1 and type 2 diabetes by enhancing the functioning of the pancreatic islet cells.

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