Anti Hair Loss Somatomedin hypothesis Anti Aging HGH Without Side
There are primarily two theories as to how hGH 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. 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.
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