Pfizer Genotropin

Content: Somatropin

Use: Subq injection

Dose: 16 IU Goquick pen

There are primarily two theories as to how hGH (human growth hormone) exerts its growth promoting effects. The first theory is called the Dual Effector theory. The second theory is called the Somatomedin (“mediator of growth”) Hypothesis. Both theories are fairly strait forward. Let’s start with the Dual Effector theory.

The Dual Effector theory states that GH itself has anabolic effects directly on body tissues. This theory has been supported by studies looking at the effects of injecting GH directly into growth plates. Genetically altered strains of mice have also help to support this theory. When comparing mice that genetically over express GH and mice that over express insulin-like growth factor-1 (IGF-1), GH mice are larger. Those who support the dual effector theory site this evidence. Interestingly, when IGF-1 antiserum (it destroys IGF-1) is administered concomitantly with GH, all of the anabolic effects of GH are abolished. Clearly IGF-1 has got to be involved somewhere between the pituitary and the target tissue (i.e. muscle). The Somatomedin hypothesis clears things up somewhat.

The Somatomedin hypothesis states that GH exerts its growth promoting effects through IGF-1. More specifically, GH is first released from the pituitary and then travels to the liver and other peripheral tissues where it causes the synthesis and release of IGFs. IGFs work as endocrine growth factors, meaning that they travel in the blood to the target tissues after being released from cells that produced it, specifically the liver in this case. Many studies have been performed showing that animals that are GH deficient, systemic IGF-1 infusions lead to normal growth. Admittedly, the effects are similar to those observed after GH administration. In fact, additional studies have shown IGF-1 to be greatly inferior as an endocrine growth factor requiring almost 50 times the amount to exert that same effects of GH. Recently rhIGF-1 has become widely more available and is currently approved form the treatment of HIV associated wasting. This increased availability allowed testing of this hypothesis in humans. Studies in human subjects with GH insensitivity (Laron syndrome) have consistently validated the somatomedin hypothesis (Rank, 1995; Savage, 1993). These results indicate that although IGF-1 might be the mediator of GH effects, it’s not as simple as just getting the liver to release IGF-1.