IGF’s and Their Role in Your Growth Hormone Pathway

by Erik Tremblay

IGF’s and Their Role in Your Growth Hormone Pathway

When we talk about our product that started it all;TEST Fx™, we like talk about it’s great effects at increasing circulating IGF levels as one of the primary anabolic effects it exerts. However, many fail to understand the significance of IGF’s and their role in a pathway that is tied to a hormone that produces some of the most anabolic effects ever studied; Growth Hormone.

Insulin-Like Growth Factors are chemical mediators in the Growth Hormone pathway that act directly on receptors located on cell surfaces to exhibit anabolic effects. IGF’s are highly similar to in structure to insulin (hence where the name comes from) and are separated into two classes based on the receptors they are able to interact with; IGF-1s and IGF-2s. While both these molecules are extremely similar in structure to each other, they do differ enough to effect what receptors they are able to interact with; IGF-1s bind to only the IGF-1 receptor while IGF-2s can actually bind both the IGF-1 and IGF-2 receptor. Below we’ll look at what types of effects these molecules produce and how they’re tied into Growth Hormone.

IGF-1 Structure

IGF-2 Structure

(source: https://en.wikipedia.org/wiki/Insulin-like_growth_factor_1, https://en.wikipedia.org/wiki/Insulin-like_growth_factor_2 )

What Are IGF-1s

The primary focus of this article will be on IGF-1s as these are the most important molecules when it comes to adult growth. IGF-1s are produced primarily by the liver and secreted into the blood to circulate around the body where it binds to receptors on all different types of cells ranging from muscle tissue cells to bone and skin cells. IGF-1s are produced by the liver when Growth-Hormone is secreted from the anterior pituitary gland and binds to the liver signaling to being production of IGF-1s. Once produced, these IGF-1s are secreted and travel around the body where they either bind to IGF-1 receptors, insulin receptors, or what are known as Insulin-Like Growth Factor Binding Proteins. These proteins, IGFBP-3 being the most abundant, bind to IGF’s and block their ability to act on either IGF-1 or Insulin receptors so they eliminate any effects the molecule would produce. This is a checks and balance system in the body to maintain it at homeostasis. However, the IGF-1s that do not bind this protein will eventually either bind to the IGF-1 receptor or Insulin receptor, both having anabolic effects.

Role Of The Insulin Receptor

The binding of IGF-1s to the insulin receptor increases the cells ability to take-in glucose to generate ATP. If insulin receptors are not bound by any molecules (IGFs or Insulin itself), glucose cannot enter the cell. So since IGF-1s have such a structural similarity to Insulin, they are able to bind the insulin receptor with some affinity and increase carbohydrate absorption and metabolism by the cells they interact with.

Role of The IGF-1R

The IGF-1 receptor (IGF-1R) is where the fun starts to happen as this receptor is associated with signaling the beginning of a intra-cellular chemical pathways within the cell it binds to that exerts anabolic effects. Once bound by IGF-1, IGF-1R can initiate several different signaling transduction pathways within the cell with the two most important being the AKT signaling pathway and the mTOR pathway. Lets take a look at what these two pathways entail:

(source: https://lookfordiagnosis.com/mesh_info.php?term=Insulin-Like+Growth+Factor+Binding+Protein+2&lang=1)

 The AKT signaling pathway is a major player in not only cell growth and proliferation, but an inhibitor to the programmed cell-death pathway known as apoptosis. Cell growth and proliferation is attributed to the pathways ability to increase protein synthesis within the cell while the blocked cell death is attributed to the pathways ability to disrupt cell death in G1 and G2 phases of the cell life cycle by regulating factors such as Nuclear Factor-κB, Bcl-2 family proteins, master lysosomal regulator TFEB and murine double minute 2 (MDM2).

The pathway associated with mTOR is another major one in regulating the growth of the cell. IGF-1R stimulation regulates the phosphatidylinositol-3 kinase (PI3K) pathways which one of the most prominent being the mTOR pathway (mammalian target of rapamycin. This pathway has the same effects as the AKT, stimulating cell growth and proliferation mostly by increasing protein synthesis and disrupting apoptosis pathways.

By disrupting apoptosis pathways and increasing protein synthesis, IGF-1Rs ability to affect signal transduction pathways once bound by IGF-1 allows it to act directly on cells of the body to increase growth. When these receptors are bound on muscle tissue to increase growth and protein synthesis, major strength and mass gains are inevitable.

How Does TEST Fx™ Work On IGF-1 Levels?

TEST Fx™ contains two highly effective compounds that work to increase natural IGF-1 production. DHEA, Dehydroepiandrosterone, is a highly studied compound that has repeatedly shown it’s ability to increase IGF-1 levels[1][2]. This is due to the compounds ability to bind directly to androgen receptors and stimulate the production of IGF-1s by the liver while decreasing the presence of IGFBP’s which inhibit IGF-1s which we talked about earlier in the article. This is combined with Deer Antler which actually contains IGF-1s by itself so it’s not only a natural source of IGF-1, but also contains other amino-acids and compounds such as Glucosamine, Chondroitin And Collagen.


IGF-2s are encoded by the IGF2 gene and are seen most beneficial in the early development of humans, especially during the gestational period. They have the ability to act on both IGF-1Rs and IGF-2Rs so they can exert the anabolic effects IGF-1s do. However, they have a higher affinity for the IGF-2 receptor which cannot act on transduction signaling pathways within cells which is why they are not very important after early development.



[1] Effect of DHEA supplementation on serum IGF-1, osteocalcin, and bone mineral density in postmenopausal, glucocorticoid-treated women. Papierska L1, Rabijewski M, Kasperlik-Załuska A, Zgliczyński W. doi: 10.2478/v10039-011-0060-9.


[2] Yen, S.S.C. et al (1995) "Replacement of DHEA in aging men and women" Ann NY Acad Sci 774: 128-42.

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