Therapeutic aspects of growth hormone and insulin-like growth factor-I

[liftsiron]

Review
Diabetes Obes Metab

. 2007 Jan;9(1):11-22.
doi: 10.1111/j.1463-1326.2006.00591.x.
Therapeutic aspects of growth hormone and insulin-like growth factor-I treatment on visceral fat and insulin sensitivity in adults
K C J Yuen 1 , D B Dunger
Affiliations

PMID: 17199714 DOI: 10.1111/j.1463-1326.2006.00591.x

Abstract

Growth hormone (GH) is generally considered to exert anti-insulin actions, whereas insulin-like growth factor I (IGF-I) has insulin-like properties. Paradoxically, GH deficient adults and those with acromegaly are both predisposed to insulin resistance, but one cannot extrapolate from these pathological conditions to determine the normal metabolic roles of GH and IGF-I on glucose homeostasis. High doses of GH treatment have major effects on lipolysis, which plays a crucial role in promoting its anti-insulin effects, whereas IGF-I acts as an insulin sensitizer that does not exert any direct effect on lipolysis or lipogenesis. Under physiological conditions, the insulin-sensitizing effect of IGF-I is only evident after feeding when the bioavailability of circulating IGF-I is increased. In contrast, many studies in GH deficient adults have consistently shown that GH replacement improves the body composition profile although these studies differ considerably in terms of age, the presence or absence of multiple pituitary hormone deficiency, and whether GH deficiency was childhood or adult-onset. However, the improvement in body composition does not necessarily translate into improvements in insulin sensitivity presumably due to the anti-insulin effects of high doses of GH therapy. More recently, we have found that a very low dose GH therapy (0.1 mg/day) improved insulin sensitivity without affecting body composition in GH-deficient adults and in subjects with metabolic syndrome, and we postulate that these effects are mediated by its ability to increase free 'bioavailable' IGF-I without the induction of lipolysis. These results raise the possibility that this low GH dose may play a role in preventing the decline of beta-cell function and the development of type 2 diabetes in these "high risk" subjects.

[Kluso]

Interesting. I was wondering what they were considering low dose GH in the other studies you posted. I’m assuming they are all related and 0.1mg/day is what they were referring to in the other studies as well? What’s so interesting to me is that one iu equals 0.33mg. So basically 0.33 or 1/3 iu per day. Normal average production is around 1.3-1.5mg per day. When we start using hgh our own production stops. Timing of the injection is important also. This is why many used to use peptides 15min before an hgh injection. It basically tricks the body into thinking your body produced the exo hgh and you ride the pulse created by the peptides. If we take an exo hgh injection you can ride that natural pulse if you are extremely lucky in your timing. But most likely within a few days your own production will stop. This study would appear to suggest that a low dose won’t cause the body to stop its own production and may in fact be additive. Do you know when they were injecting the .1mg hgh during the day? My speculation would be first thing in the morning as to not interfere with the biggest natural pulses during the night but maybe not.

[Kluso]

Either that or the individuals weren’t even producing 0.1mg hgh naturally? Would need to know that as well since we could be shutting down natural production that may be more than 0.1mg per day. And end up reducing our total hgh per day.