The modern application of bio-engineered myostatin-blocking peptides, MYOPEP, in Aesthetic and Therapeutic medicine

Learning Objectives:

Introduction to the newly discovered, bio-engineered peptides as an effective inhibitor of myostatin, the growth and differentiation factor 8 (GDF8) found in muscle receptor sites.

An insight into the application protocols and successful clinical trials demonstrating significant fat loss and muscle gain for body sculpting and slimming.

 

Abstract:

Obesity is associated with a metabolic imbalance that produces increased adipose tissue mass caused by a combination of hypertrophy and hyperplasia of adipocytes.

Importantly, adipose tissue is itself a critical regulator of systemic metabolism, which suggests that modulation of adipogenesis should have a greater systemic impact than merely altering adipose tissue mass.

Adipocytes originate from pluripotent progenitor cells (precursor stem cells) characteristic of the adipocyte lineage. A group of factors and cytokines, not fully defined, initiate a cascade of differentiation processes in which a stem cell commits to a specific lineage, for example, to become a 'preadipocyte'.

Further signals continue the progression by inducing proliferation and finally differentiation into lipid-laden adipocytes.

Myostatin, also known as growth and differentiation factor 8 (GDF8), is a member of the TGFbeta super family. Myostatin inhibits the recruitment of mesenchyme stem cells away from the musculoskeletal pathway causing an intermission to myogenesis, and conversely promotes the differentiation of multipotent mesenchymal cells into the adipogenic lineage.

A newly discovered bio-engineered peptide MYOPEP – a proprietary amino acid complex developed as an isoform of the follistatin protein – is capable of inducing a pharmaceutical grade effect in human muscle and adipose fat function.

The peptide functions by deactivating the specialized enzymes, myostatin to significantly block adipogenesis while simultaneously enhance myogenesis with limited toxicity in animals and humans. Metabolism or glycolysis (sugar metabolism) rises, forcing fat to be broken down into sugar to feed muscular action and growth. It ultimately causes hypertrophic effect in which muscles begin to grow larger, appear more defined and have greater strength.

Specifically designed to engender a self-limiting characteristic, the bio-engineered peptide MYOPEP is metabolized after a specific period of time, thereby eliminating the possibility of an interminable signaling of muscle growth. In addition, this critical element of self-regulation allows the peptide application to be varied and modulated according to result feedback.

One subcutaneous injection of MYOPEP at the abdominal area in a week over a period of two months has shown significant fat loss in the first twelve subjects trialed and a significant drop in glucose metabolic parameters.

This myostatin-blocking peptide formulation is potentially an integral part of muscular enhancement and sports medical rehabilitation, as well as the therapeutic care for type 2 diabetes related weight issues, obesity related weight loss, aging related muscle wasting and cerebral palsy.

Protocol:

Three subcutaneous administration of one vial each time at the abdominal area in the first week. Frequency of administration can be reduced in the following weeks based on result feedback.


References:

  • Division of Endocrinology, Charles R. Drew University, Los Angeles, CA 90059; Division of Endocrinology, Washington University School of Medicine, St. Louis, MO 63110; University of Toronto, Toronto, Ontario, M5S1A1 Canada; and Karolinska Institutet, Stockholm, SE-171 76 Sweden
  • Taylor WE, Bhasin S, Artaza J, Byhower F, Azam M, Willard DH Jr, Kull FC Jr, Gonzalez-Cadavid N. Myostatin inhibits cell proliferation and protein synthesis in C2C12 muscle cells.
  • Haidet AM, Rizo L, Handy C, Umapathi P, Eagle A, Shilling C et al. Long-term enhancement of skeletal muscle mass and strength by single gene administration of myostatin inhibitors. Proc Natl Acad Sci USA 2008; 105: 4318–4322.

 

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