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Growth Hormone administration results in an increase in lean body mass (LBM)?
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Growth Hormone administration results in an increase in lean body mass (LBM)? - 02-02-2013, 03:27 PM

by datbtrue

GH increases [resting energy expenditure ], lipolysis, and lipid oxidation, xxx, xxx.



Resting Energy Expenditure (REE) in both GH deficient and healthy adults, has been found to be increased by acute growth hormone (GH) administration,1 2. The converse has also been found to be true. REE is reduced by acute GH receptor blockade in normal subjects 3.

A quantification of what this means in practical terms may be found in a meta-analysis of seven human studies by Liu et al.. This analysis indicated that basal metabolic rate was significantly higher in GH-treated subjects than in those not treated with GH, by an average of 141 kcal/day (range: 69–213 kcal/day). Resting heart rate as well was found to be significantly higher in GH-treated subjects by 3.8 beats/min (range: 0.2–7.4 beats/min.). 5 Although neither the amount of GH administered nor pattern was mentioned in the meta-study it is safe to assume that the average dosing was not high supra-physiological and the pattern was all at once (or non pulsatile).

For comparison we have a well constructed placebo-controlled, double-blind, cross-over study wherein 6 healthy young women were administered a high supra-physiological dose of 12iu of GH (Norditropin) per day for 14 days. GH increased resting energy expenditure from 1500 +/- 100 kcal/day (placebo) to 1710 +/-60 kcal/day. 6 So that would be an increase of 210 kcal/day or 14%. Although there is variability reported in both studies perhaps we should allow ourselves to conclude, that exogenous GH administered into healthy individuals and deficient individuals increases resting energy expenditure. There appears to be a greater amount of energy expenditure at higher dose. This is all without regard to dosing pattern.

A subsequent study involving young, healthy, lean men who were administered a medium supra-physiological dose of 6iu of GH (Norditropin) at 10:00 PM daily for 14 days gives us some information on energy expenditure as it relates to time. The measurable increase in energy expenditure immediately following the GH administration period was 8.3%. For the entire night period the increase in energy expenditure was 5.3%. As night became day and the subjects were farther removed from the previous nighttime administration the measurable increase in daytime energy expenditure was 3.9%.1. Based on this study, it appears that the increase in energy expenditure is most acute in the time period following administration.

What is Responsible for GH's inducement of increased resting energy expenditure?

Resting Enegy Expenditure (REE) is strongly correlated to lean body mass (LBM), so any change in LBM will result in a parallel change in REE. However, GH also directly stimulates REE, as the GH-induced increase in REE persists after correction for the increase in LBM 2. There is still no consensus on the precise mechanisms responsible for the GH's increase in REE. GH has been found to increase skeletal muscle uncoupling protein-3 4 and this is often advanced as a possible explanatory factor in the GH-induced REE increase. Yet with the knowledge that "T3 promotes increased thermogenesis in part by promoting mitochondrial energy uncoupling in skeletal muscle" 7 we are led back to argument that the explanation is GH's well established stimulation of conversion of peripheral thyroxine (T4) to tri-iodothyronine (T3) the active thyroid hormone. - Jorgensen JO, Growth hormone administration stimulates energy expenditure and extrathyroidal conversion of thyroxine to triiodothyronine in a dose-dependent manner and suppresses circadian thyrotrophin levels: studies in GH-deficient adults, Clin Endocrinol (Oxf). 1994;41(5):609–14

Is that THE explanatory mechanism?

The science of today seems to reason that it could not be so in whole, only in part. Their experimental data seems to indicate that the approximately 10% increase in T3 levels as a result of GH is insufficient to account for the observed GH-induced 10–20% increase in REE. 8

I think they are missing something. I think that Growth Hormone's effect on thyroid hormone metabolism particularly at the periphery is THE primary explanatory mechanism.

I acknowledge that there are secondary mechanisms , such as GH's increase of resting cardiac output 9 and blood flow in and around organs and skeletal muscle. 10,11 I also am open to the probability that those users of very high elevated GH doses put themselves in a state that mimics acromegaly's increased futile glucose cycling (increased basal hepatic glucose production/insulin resistance) as a significant expenditure of energy. It is not my intent to discuss the unhealthy state of professional bodybuilders. Elsewhere I may point to high dose GH's failure to have any effect on intramuscular fat deposits which spares muscle fat as body fat drops. Most people prefer to see their hero's as flexor's of pure muscle. I don't need to abuse their illusions. I only note it here because I won't discuss so much the flirting with acromegaly mechanisms.

Back to my point. I believe that what science is missing is a look at amplification or deamplification of T3 inside the cell. By focusing only on the increased conversion of T4 to T3 they miss what happens inside the cell to make T3 more or less effective. They miss reverse T3.

Jorgensen (1994) was the first study to find a correlation between GH administration and an increase in T4 to T3 conversion. What they didn't seem to fully appreciate in 1994 was the significance of the drastic decrease in reverse T3 (rT3). Notice from the chart that serum rT3 concentrations markedly decreased in a GH dose-dependent manner.

Name: Gh-T3-rT3.jpg Views: 170 Size: 145.8 KB

What is Reverse T3?

Simply put reverse T3 is an inactive form of T3. It is a metabolic "throttle" down mechanism. Metabolism is slowed when more T3 is inactivated into reverse T3. Metabolism would be expected to rise when less T3 is inactivated into reverse T3. The conversion of T4 to T3 and the inactivation of T3 to reverse T3 is accomplished through the work of several enzymes. It is these enzymes that growth hormone affects and it is for that reason that we will examine this area in detail.

In humans, peripheral (and by that we just mean away from the main hormone producing organs) thyroid hormone metabolism is mediated by three enzymes (called: iodothyronine deiodinases). They are D1, D2, and D3. D1 is present in liver, kidney, and thyroid and plays a key role in the conversion of T4 to T3 and in the catabolism of reverse T3. D2 is present in brain, pituitary, thyroid, and skeletal muscle and also converts T4 by outer ring deiodination to T3 (i.e. removal of an iodine). D3 is present in brain, skin, placenta, pregnant uterus, and fetal tissues and inactivates T4 and T3 by inner ring deiodination to rT3 and 3,3'-diiodothyronine (i.e. removal of a different iodine), respectively.

Problems result when you have an Overactive D3 enzyme and an Underactive D2/D1 enzyme. As I will eventually discuss GH rescues these problems.


Overactive D3 enzyme - D3 catalyzes the conversion of plasma and cellular T4 and T3 to the inactive metabolites rT3 and T2, respectively, decreasing the nuclear pool of T3 available to occupy TR (thyroid receptor). - Endocr Rev. 2008 December; 29(7): 898–938.

Take a look...D3 is dismantling T3 into T2 before it can get to the nuclear receptor &amp; it is converting T4 to rT3 before it can convert to T3. There is no clogging of a receptor just a low amount of available T3 in the nucleus.

Name: A.jpg Views: 173 Size: 82.0 KB

Underactive D2/D1 enzyme - D2 catalyzes the conversion of cellular T4 to T3 In D2-expressing cells, the nuclear pool of T3 available to the thyroid receptors (TRs) originates from both plasma T3 and T3 generated via D2.

Here is what should happen when D2/D1 is acting properly.

Name: B.jpg Views: 175 Size: 87.8 KB


There may be a misconception that the primary throttling of metabolism comes from reverse T3 blocking receptors. Perhaps the primary mechanism is the depletion of nuclear T3 pools as described above and modulation of the ATP/ADP ratio as briefly described below.

The following study does indicate that reverse T3 does bind to receptors just not T3 receptors. "The data suggest that... there exist specific high affinity, low capacity nuclear rT3-binding sites in rat and pork liver which are distinct from the nuclear T3 receptors" - Specific Nuclear Binding Sites of Triiodothyronine and Reverse Triiodothyronine in Rat and Pork Liver: Similarities and Discrepancies, Wiersinga, W Endocrinology June 1, 1982 vol. 110 no. 6 2052-2058

Perhaps this binding to reverse-T3 binding sites plays a role in bringing about the effect described below.


The really interesting possibility is that rT3 (reverse T3) actually has an inverse biological activity. In the study Adverse effects of reverse triiodothyronine on cellular metabolism as assessed by 1H and 31P NMR spectroscopy, Ryoji Okamoto, Dieter Leibfritz, Res Exp Med (1997) 197: 211–217 they concluded:

Recently, T3 supplement therapy has been focused on [sic] in the fields of transplantation and liver surgery. The rationale for T3 administration seems to be based on the assumption that organ function would be impaired in the absence of T3 where rT3 plays only a minor role as a "silent" byproduct of T4. However, our results may indicate that rT3 itself has adverse biological effects, at higher acidity in particular, although its mechanism of action remains to be clarified.

What they did was incubate 3T3 cells for several hours in either T3 or rT3. They did this at two different pH levels. They looked at the ATP/ADP ratio and found that T3 increased it from 6.9 to 8.4 while rT3 decreased it from 6.9 to 6.1 at a cellular pH of 7.4. When the same experiment was carried out in a cellular pH of 6.1 ATP/ADP ratio declined in controls but T3 saved the day and pushed the ATP/ADP ratio up, while rT3 pushed the ATP/ADP ratio down.

So in two different environments T3 increases ATP which is energy while rT3 decreases ATP which is "fatigue".

These cells that were used were not altered enzymatically by some stressful in vivo condition and thus it is not possible for the explanation to be "a depletion of nuclear T3 pools" as described above. rT3 is bringing about anti-T3 effects in regard to ATP all by itself. It isn't just preventing T3 effects it seems to be actively triggering anti-T3 effects and this may be via binding to reverse-T3 binding sites.


To reiterate, reducing the activity of the D3 enzyme and boosting the activity of the D1 enzyme will have a positive impact on metabolism and resting energy expenditure. The D3 inactivates T3 in peripheral tissue and D1 converts T4 to T3. Now the following study demonstrated that growth hormone infusion (i.e. elevations) alone only did half the job of increasing metabolism. It did so via suppression of D3 activity which as we know reduces inactivation of T3. "Suppression of D3, but not stimulation of D1, also occurred in response to administration of rhGH." - Endocrine and Metabolic Effects of Growth Hormone (GH) Compared with GH-Releasing Peptide, Thyrotropin-Releasing Hormone, and Insulin Infusion in a Rabbit Model of Prolonged Critical Illness , Weekers , Endocrinology 145(1):205–213

Now the use of of a pulsatile approach, GHRP-2 coupled with use of a thyroid precursor (to insure that the depleted subjects were repleted... probably does not apply to normal subjects) was able to "augment and depressed the catalytic activity of hepatic D1 and D3" respectively. In other words D3 activity was decreased which reduced the inactivation of T3, leaving more T3 available and unlike straight GH elevations, increase D1 activity which meant increased conversion of T4 to T3. - Weekers (fully cited above)


1. Hansen M, Effects of 2 wk of GH administration on 24-h indirect calorimetry in young, healthy, lean men. Am J Physiol Endocrinol Metab. 2005;289(6): E1030–8

2. Stenlof K, . Effects of recombinant human growth hormone on basal metabolic rate in adults with pituitary deficiency. Metabolism. 1995;44(1):67–74

3. Moller L, Impact of growth hormone receptor blockade on substrate metabolism during fasting in healthy subjects. J Clin Endocrinol Metab. 2009;94(11):4524–32

4. Pedersen SB, Regulation of uncoupling protein-2 and -3 by growth hormone in skeletal muscle and adipose tissue in growth hormone-deficient adults. J Clin Endocrinol Metab. 1999;84(11):4073–8

5. Liu H, Systematic review: the effects of growth hormone on athletic performance. Ann Intern Med. 2008;148(10):747–58

6. Meller N., Impact of 2 weeks high dose growth hormone treatment on basal and insulin stimulated substrate metabolism in humans, Clinical Endocrinology (1993) 39, 577-581

7. Lebon, V., Effect of triiodothyronine on mitochondrial energy coupling in human skeletal muscle, J. Clin. Invest. 108:733–737 (2001)

8 - Wolthers T, 1996 Calorigenic effects of growth hormone: the role of thyroid hormones. J Clin Endocrinol Metab 81: 1416–1419

9 - Thuesen L, 1994 Short and long-term cardiovascular effects of growth hormone therapy in growth hormone deficient adults. Clin Endocrinol (Oxf) 41:615–620

10 - Boger RH, 1996 Nitric oxide may mediate the hemodynamic effects of recombinant growth hormone in patients with acquired growth hormone deficiency. A double-blind, placebo-controlled study. J Clin Invest 98:2706 –2713

11 - Jorgensen JO, 1989 Beneficial effects of growth hormone treatment in GH-deficient adults. Lancet 1:1221–1225

Last edited by DatBtrue; 7th June 2012 at 08:12 AM.

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