Does GH lead to diabetes to someone pre-disposed?

[BuffGuy]

I am NOT diabetic, thank God.

However, it DOES run in my family.

Would GH lead to diabetes (or increase the chances) to one pre-disposed to diabetes?

[einstein1905]

GH can increase insulin sensitivity, but I see no reason why it would hasten your progress towards type II diabetes. GH/IGF-1 both have the ability to make you more insulin sensitive while you're using them. You have no signs of it now? No hyperglycemia? Have you monitored BG over a period? If you're relatively young and lean, even if you're predisposed genetically, I wouldn't worry about it for now.

[BuffGuy]

Thanks for the reply.

Nah, I'm perfectly fit and healthy now...no signs of diabetes.

[longhornDr]

Secondary type II diabetes is a common side effect of high levels of GH, exogenous or endogenous, it is reversed when GH levels are returned to normal. GH causes insulin resistance (which is why insulin is often used in conjunction with GH).

In theory I suppose you could blow out your pancreas by staying on high doses of GH for extended periods of time....similiar to what happens to obese people predisposed to type II diabetes.

[einstein1905]

I've also read GH will cause varying degrees of insulin resistance, but I have measured my BG prior to starting GH with the same simple carb intake post w/o and again after I'd started GH in the same situation....My BG was much lower while I was using GH, while taking in the same amount of simple carbs at the same time point post w/o. This wasn't an isolated event either.

I agree that the majority of the literature says increased GH levels will likely cause increased insulin resistance, but it's not a given....clearly it had the opposite effect with me.

JB reported to have considerably lower BG after using IGF-1 post w/o compared to the same situations while not using IGF-1.

Since GH increases hepatic IGF-1, there is potential for insulin sensitivity to be skewed in either direction IMO.

[longhornDr]

I've also read GH will cause varying degrees of insulin resistance, but I have measured my BG prior to starting GH with the same simple carb intake post w/o and again after I'd started GH in the same situation....My BG was much lower while I was using GH, while taking in the same amount of simple carbs at the same time point post w/o. This wasn't an isolated event either.

I agree that the majority of the literature says increased GH levels will likely cause increased insulin resistance, but it's not a given....clearly it had the opposite effect with me.

JB reported to have considerably lower BG after using IGF-1 post w/o compared to the same situations while not using IGF-1.

Since GH increases hepatic IGF-1, there is potential for insulin sensitivity to be skewed in either direction IMO.

Were you taking anabolics at the same time?

Did you measure your BG throughout the day or just post-workout? After a workout the anabolic effects of IGF-1 could be overpowering the hyperglycemic actions of GH....or you could be having a rebound effect caused by hyper-secretion of insulin in repsonse to hyperglycemia from your post-workout carbs. Did you take several BG measurements after your PWO meal?

[einstein1905]

Were you taking anabolics at the same time?

Did you measure your BG throughout the day or just post-workout? After a workout the anabolic effects of IGF-1 could be overpowering the hyperglycemic actions of GH....or you could be having a rebound effect caused by hyper-secretion of insulin in repsonse to hyperglycemia from your post-workout carbs. Did you take several BG measurements after your PWO meal?

My measurements were 30 min after my shot (carbs had already been ingested as had pwo shake) and again roughly 2 hrs post injection. I've measured at these times both while using AAS and while not using, but still using GH. I didn't see any real trend that would tell me there was a difference between AAS use or not, but I know, in general, there should be.
I also measured BG in the AM at similar time points (insulin in the AM too for awhile).

I agree that the post w/o carbs could definitely be playing a role in boosting endogenous insulin too....the times at which I measured BG won't be able to confirm that, because I never measured post injection/precarb intake.

In theory, with IGF-1 LR3, with its long active life (relative to IGF-1), it could play a role in increasing insulin sensitivity while it's present. Taking GH in conjunction with LR3 would.....have what net effect (obviously dependent on dose) on insulin sensitivity?
Also, how exactly does GH mediate insulin insensitivity?

Thanks for your reply...I appreciate you taking the time to answer.

[flexshack]

My measurements were 30 min after my shot (carbs had already been ingested as had pwo shake) and again roughly 2 hrs post injection. I've measured at these times both while using AAS and while not using, but still using GH. I didn't see any real trend that would tell me there was a difference between AAS use or not, but I know, in general, there should be.
I also measured BG in the AM at similar time points (insulin in the AM too for awhile).

I agree that the post w/o carbs could definitely be playing a role in boosting endogenous insulin too....the times at which I measured BG won't be able to confirm that, because I never measured post injection/precarb intake.

In theory, with IGF-1 LR3, with its long active life (relative to IGF-1), it could play a role in increasing insulin sensitivity while it's present. Taking GH in conjunction with LR3 would.....have what net effect (obviously dependent on dose) on insulin sensitivity?
Also, how exactly does GH mediate insulin insensitivity?

Thanks for your reply...I appreciate you taking the time to answer.

are you saying that gh is reported to reduce insulin sensitivity, while igf-1 is supposed to do the opposite? that seems a little odd.

[einstein1905]

are you saying that gh is reported to reduce insulin sensitivity, while igf-1 is supposed to do the opposite? that seems a little odd.

IGF-1, after all, is "insulin -like growth factor". It has ~50% homology to insulin itself. Their respective receptors share a great deal of homology, and the signaling cascades that ensue after their bindings invlove many of the same factors as well. There were some clinical studies that tested the effecacy of IGF-1 in treatment of both type I and II diabetes.
I'll quote from a book entitled "The IGF system" by Drs Rosefeld and Roberts:

IGF-1 shares many structural and functional similarities to its close ho,olog, insulin. Dysregulation of the GH-IGF-1 axis in type I diabetes mellitus is clear, and data support a degree of disregulation in type II diabetes as well. Compelling data support that the deficiency of IGF-1 in poorly controlled type I diabetes results from inadequate hepatic insulinization although a direct relationship between low IGF-1 levels and either insulin resistance or por glycemic control has been presumed, but not proven. The pharmacokinetics of IGF-1 differ dramatically from those of insulin, and as such make understanding the pharmacodynamics of the drug somewhat obscure. the effects of rhIGF-1 on glycemic control are gradual in onset and are associated with lowering of endogenous insulin despite improvement of blood glucose concentration. .......Clinical trials of IGF-1 in both type I and type II diabetes and in patients with severe insulin resistance of different phenotypes support the concept that this agent is of therapeutic value in at least some patients

Here is one of the earlier clinical studies comparing insulin to IGF-1:

N Engl J Med. 1987 Jul 16;317(3):137-40. Related Articles, Links


Short-term metabolic effects of recombinant human insulin-like growth factor I in healthy adults.

Guler HP, Zapf J, Froesch ER.

Insulin-like growth factor I (IGF I) is structurally similar to insulin and shares many of its biologic properties. We compared the short-term metabolic effects of recombinant IGF I (100 micrograms [13.3 nmol] per kilogram of body weight) and insulin (0.15 IU [1 nmol] per kilogram) in eight healthy volunteers (four men and four women). The hypoglycemic responses to both hormones were nearly identical in the doses used. The lowest blood glucose levels were reached after 30 minutes: 1.98 +/- 0.44 mmol per liter after IGF I and 1.78 +/- 0.29 after insulin. On a molar basis, IGF I was only 6 percent as potent as insulin in the production of hypoglycemia. Insulin also inhibited lipolysis more effectively than IGF I. Levels of epinephrine, norepinephrine, growth hormone , glucagon, and cortisol responded similarly to both agents. The hypoglycemia produced by IGF I is probably due to the supraphysiologic concentrations of the free peptide that result from its rapid intravenous injection. Fifteen minutes after injection, the serum level of IGF I increased from 144 +/- 38 ng per milliliter at base line to 424 +/- 56, of which 80 percent was free in the plasma (not bound to IGF carrier proteins). The determination of whether any of the short-term metabolic effects of IGF I have any clinical application will require further investigation.


Keep in mind that substituting IGF-1 for insulin can still cause insulin dependence(assumed) just as taking in exogenous insulin may very well lead to insulin dependence. I'll read up more on both GH and IGF-1's detailed effects on insulin sensitivity. I have so many books here....how did the old timers ever learn anything without the internet??

[flexshack]

Levels of epinephrine, norepinephrine, growth hormone , glucagon, and cortisol responded similarly to both agents.

HOW ARE THESE LEVELS AFFECTED? JUST CURIOUS.

Keep in mind that substituting IGF-1 for insulin can still cause insulin dependence(assumed) just as taking in endogenous insulin may very well lead to insulin dependence.

DO YOU MEAN, "TAKING IN EXOGENOUS INSULIN MAY VERY WELL LEAD TO INSULIN DEPENDENCE"? I AM A LITTLE CONFUSED HERE. JUST A TYPO?

I'll read up more on both GH and IGF-1's detailed effects on insulin sensitivity. I have so many books here....how did the old timers ever learn anything without the internet??

VERY TRUE. DEDICATION AND PATIENCE I GUESS.

btw, thanks for the awesome post as usual.

[einstein1905]

btw, thanks for the awesome post as usual.

Thanks for catching the typo...I fixed it.

All of the hormones that you mentioned will go down in response to insulin (or IGF-1).
Long term hypoglycemia will increase the release of GH and cortisol (I'm not sure on this....just a theory, but GH may be released due to its ability to increase the release of FFAs from adipocytes to serve as a energy source). Cortisol would be to catabolize muscle to free amino acids to serve as "fuel" upon conversion to Acetyl CoA and entry into the mitochondria. Glucagon has the exact opposite effects of insulin, so it serves to release glucose from intracellular glycogen stores. Epi and norepi serve as metabolic catalysts as far as the others are concerned in this context.

The following is from endotext.com:

METABOLIC EFFECTS OF GROWTH HORMONE

Glucose Homeostasis and Lipid Metabolism

The involvement of the pituitary gland in the regulation of substrate metabolism was originally detailed in the classic dog studies by Houssay (24). Fasting hypoglycaemia and pronounced sensitivity to insulin were described as salient features of hypophysectomised animals. These symptoms were readily corrected by administration of anterior pituitary extracts. It was also noted that pancreatic diabetes was alleviated by hypophysectomy. Finally, excess of anterior pituitary lobe extracts aggravated or induced diabetes in hypophysectomised dogs.

Luft et al. (25) clearly demonstrated the glycaemic control to deteriorate following exposure to a single supraphysiological dose of human GH in hypophysectomised adults with type 1 diabetes mellitus. Somewhat surprisingly, only modest effects of GH on glucose metabolism were recorded in the first metabolic balance studies involving adult hypopituitary patients (26, 27).

More recent studies on glucose homeostasis in GH deficient adults have generated results, which at first glance may appear contradictory. Insulin resistance may be more prevalent in untreated GH deficient adults (28, 29), whereas the impact of GH replacement on this feature seems to depend on the duration and the dose. Below, some of the metabolic effects of GH in human subjects, with special reference to the interaction between glucose and lipid metabolism, will be reviewed.

Studies In Normal Adults

Almost forty years ago it was shown that infusion of high dose GH into the brachial artery of healthy adults reduced forearm glucose uptake in both muscle and adipose tissue (30). This was parallelled by a drop in RQ and an increase in muscle uptake of FFA, both of which suggest oxidation of FFA by the muscle. This pattern was opposite that of insulin, and co-administration of insulin and GH resulted in only minimal changes in net fluxes of glucose and FFA across the forearm bed. These studies clearly indicated direct insulin antagonistic effects of GH on muscle and adipose tissue.

The introduction of reliable radioimmunoassays for GH revealed the pulsatile and episodic nature of GH release (31) now known to be generated by alternating secretion of GHRH and SST. A GH pulse is released roughly every second hour with a mean daily secretion of 0.5 mg (32). Apart from a well-known circadian variation in terms of elevated nocturnal GH levelsduring the early hours of sleep, GH secretion is amplified during fasting and stress, whereas meals suppress GH release. We studied the metabolic effect of a physiological GH bolus in the postabsorptive state, and demonstrated stimulation of lipolysis following a lag time of 2-3 hours to be the most consistent effect (33). Plasma glucose, on the other hand exhibited only minimal fluctuations, and serum insulin and C-peptide levels remained completely stable. This was associated with subtle reductions in muscular glucose uptake and oxidation, which could reflect substrate competition between glucose and fatty acids (i.e. the glucose/fatty acid cycle). In line with this, sustained exposure to high GH levels induces both hepatic and peripheral (muscular) resistance to the actions of insulin on glucose metabolism together with increased (or inadequately suppressed) lipid oxidation. Apart from enhanced glucose/fatty acid cycling, it has been shown that GH induced insulin resistance is accompanied by reduced muscle glycogen synthase activity (34) and diminished glucose dependent glucose disposal (35). Bak et al. (34) also demonstrated insulin binding and insulin receptor kinase activity from muscle biopsies to be unaffected by GH.

Lessons From Acromegaly

Active acromegaly clearly unmasks the diabetogenic properties of GH. In the basal state plasma glucose is elevated despite compensatory hyperinsulinemia. In the basal and insulin-stimulated state (euglycemic glucose clamp) hepatic and peripheral insulin resistance is associated with enhanced lipid oxidation and energy expenditure (36). There is evidence to suggest that this hypermetabolic state ultimately leads to beta cell exhaustion' and overt diabetes mellitus (37), but a more recent study have demonstrated that the abnormalities are completely reversed after successful surgery (36). Conversely, it has been shown that only two weeks administration of GH in supraphysiological doses (8 IU/day) induces comparable acromegaloid - and reversible - abnormalities in substrate metabolism and insulin sensitivity (38).

INTERACTION OF GLUCOSE AND LIPID METABOLISM

Relatively few studies have scruntinised the exact sites of action of GH on glucose metabolism. There is no evidence of a net effect of GH on insulin binding to the receptor (34, 39), which obviously implies post receptor metabolic effects. The effect of FFA on the partitioning of intra-cellular glucose fluxes was originally described by Randle et al. (40). According to his hypothesis (the glucose/fatty acid cycle), oxidation of FFA initates an up-stream, chain-reaction-like inhibition of glycolytic enzymes, which ultimately inhibits glucose uptake. When considering the pronounced lipolytic effects of GH the Randle hypothesis remains an appealing model to explain the insulin-antagonistic effects of GH glucose metabolism. In support of this experiments have shown that co-administration of anti-lipolytic agents and GH reverses GH-induced insulin resistance. Similar conclusions were drawn from a recent study in GH deficient adults, which showed that insulin sensitivity was restored when acipimox (a nicotinic acid derivative) was co-administered with GH (41). It has, however, also been reported that GH-induced insulin resistance preceded the increase in circulating levels and forearm uptake of lipid intermediates (42). This early effect of GH on muscular glucose uptake could reflect intra-myocytic FFA release and oxidation and thus be compatible with the Randle hypothesis. It could also imply alternative (early) effects of GH. Moreover, the inhibitory effect of GH on muscle glycogen synthase activity (34) is not readily explained by substrate competition. According to the Randle hypothesis the fatty acid-induced insulin resistance will result in elevated intracellular levels of both glucose and glucose-6-phosphate. By contrast, muscle biopsies from GH deficient adults after GH treatment have revealed increased glucose but low-normal glucose-6-phosphate levels (43). Moreover, NMR spectroscopy studies in healthy adults indicate that FFA infusion results in a drop in the levels of both glucose and glucose-6-phosphate (44). The latter study did not involve GH administration, but it does challenge the Randle hypothesis and suggest that FFA may impair very early steps in glucose transporter activity (GLUT 4). The impact of GH on GLUT 4 translocation has not yet been studied in human subjects.

Implications For Gh Replacement

Regardless of the exact mechanisms, the insulin antagonistic effects may cause concern when replacing adult GH deficient patients with GH, since some of these patients are insulin resistant in the untreated state. There is evidence to suggest that the direct metabolic effects on GH may be balanced by long-term beneficial effects on body composition and physical fitness, but some studies report impaired insulin sensitivity in spite of favourable changes in body composition. There is little doubt that these effects of GH are dose-dependent and may be minimised or avoided if an appropriately low replacement dose is used. Still, the pharmacokinetics of s.c. GH administration is unable to mimick the endogenous GH pattern with suppressed levels after meals and elevations only during postabsorptive periods, such as during the night. This may be considered the natural domain of GH action which coincides with minimal beta-cell challenge. This reciprocal association between insulin and GH and its potential implications for normal substrate metabolism was initially recognised by Rabinowitz & Zierler (45) . The problems arise when GH levels are elevated during repeated prandial periods. The classic example is active acromegaly, but prolonged high dose s.c. GH administration may cause similar effects. Subcutaneous administration of GH in the evening probably remains the best compromise between effects and side effects (46), but it is far from physiological. We know and understand that hypoglycaemia is a serious and challenging side effect of insulin therapy as a consequence of inappropriately high insulin levels (during fasting). As a corollary, we must realise that hyperglycaemia may result from GH therapy. It is therefore important to carefully monitor glucose metabolism and to use the lowest effective dose when replacing adults with GH.

I've attached a diagram that shows, pretty simply, the interplay between various components of the endocrine system that are relevant here

[flexshack]

Thanks for catching the typo...I fixed it.

All of the hormones that you mentioned will go down in response to insulin (or IGF-1).
Long term hypoglycemia will increase the release of GH and cortisol (I'm not sure on this....just a theory, but GH may be released due to its ability to increase the release of FFAs from adipocytes to serve as a energy source). Cortisol would be to catabolize muscle to free amino acids to serve as "fuel" upon conversion to Acetyl CoA and entry into the mitochondria. Glucagon has the exact opposite effects of insulin, so it serves to release glucose from intracellular glycogen stores. Epi and norepi serve as metabolic catalysts as far as the others are concerned in this context.

The following is from endotext.com:

METABOLIC EFFECTS OF GROWTH HORMONE

Glucose Homeostasis and Lipid Metabolism

The involvement of the pituitary gland in the regulation of substrate metabolism was originally detailed in the classic dog studies by Houssay (24). Fasting hypoglycaemia and pronounced sensitivity to insulin were described as salient features of hypophysectomised animals. These symptoms were readily corrected by administration of anterior pituitary extracts. It was also noted that pancreatic diabetes was alleviated by hypophysectomy. Finally, excess of anterior pituitary lobe extracts aggravated or induced diabetes in hypophysectomised dogs.

Luft et al. (25) clearly demonstrated the glycaemic control to deteriorate following exposure to a single supraphysiological dose of human GH in hypophysectomised adults with type 1 diabetes mellitus. Somewhat surprisingly, only modest effects of GH on glucose metabolism were recorded in the first metabolic balance studies involving adult hypopituitary patients (26, 27).

More recent studies on glucose homeostasis in GH deficient adults have generated results, which at first glance may appear contradictory. Insulin resistance may be more prevalent in untreated GH deficient adults (28, 29), whereas the impact of GH replacement on this feature seems to depend on the duration and the dose. Below, some of the metabolic effects of GH in human subjects, with special reference to the interaction between glucose and lipid metabolism, will be reviewed.

Studies In Normal Adults

Almost forty years ago it was shown that infusion of high dose GH into the brachial artery of healthy adults reduced forearm glucose uptake in both muscle and adipose tissue (30). This was parallelled by a drop in RQ and an increase in muscle uptake of FFA, both of which suggest oxidation of FFA by the muscle. This pattern was opposite that of insulin, and co-administration of insulin and GH resulted in only minimal changes in net fluxes of glucose and FFA across the forearm bed. These studies clearly indicated direct insulin antagonistic effects of GH on muscle and adipose tissue.

The introduction of reliable radioimmunoassays for GH revealed the pulsatile and episodic nature of GH release (31) now known to be generated by alternating secretion of GHRH and SST. A GH pulse is released roughly every second hour with a mean daily secretion of 0.5 mg (32). Apart from a well-known circadian variation in terms of elevated nocturnal GH levelsduring the early hours of sleep, GH secretion is amplified during fasting and stress, whereas meals suppress GH release. We studied the metabolic effect of a physiological GH bolus in the postabsorptive state, and demonstrated stimulation of lipolysis following a lag time of 2-3 hours to be the most consistent effect (33). Plasma glucose, on the other hand exhibited only minimal fluctuations, and serum insulin and C-peptide levels remained completely stable. This was associated with subtle reductions in muscular glucose uptake and oxidation, which could reflect substrate competition between glucose and fatty acids (i.e. the glucose/fatty acid cycle). In line with this, sustained exposure to high GH levels induces both hepatic and peripheral (muscular) resistance to the actions of insulin on glucose metabolism together with increased (or inadequately suppressed) lipid oxidation. Apart from enhanced glucose/fatty acid cycling, it has been shown that GH induced insulin resistance is accompanied by reduced muscle glycogen synthase activity (34) and diminished glucose dependent glucose disposal (35). Bak et al. (34) also demonstrated insulin binding and insulin receptor kinase activity from muscle biopsies to be unaffected by GH.

Lessons From Acromegaly

Active acromegaly clearly unmasks the diabetogenic properties of GH. In the basal state plasma glucose is elevated despite compensatory hyperinsulinemia. In the basal and insulin-stimulated state (euglycemic glucose clamp) hepatic and peripheral insulin resistance is associated with enhanced lipid oxidation and energy expenditure (36). There is evidence to suggest that this hypermetabolic state ultimately leads to beta cell exhaustion' and overt diabetes mellitus (37), but a more recent study have demonstrated that the abnormalities are completely reversed after successful surgery (36). Conversely, it has been shown that only two weeks administration of GH in supraphysiological doses (8 IU/day) induces comparable acromegaloid - and reversible - abnormalities in substrate metabolism and insulin sensitivity (38).

INTERACTION OF GLUCOSE AND LIPID METABOLISM

Relatively few studies have scruntinised the exact sites of action of GH on glucose metabolism. There is no evidence of a net effect of GH on insulin binding to the receptor (34, 39), which obviously implies post receptor metabolic effects. The effect of FFA on the partitioning of intra-cellular glucose fluxes was originally described by Randle et al. (40). According to his hypothesis (the glucose/fatty acid cycle), oxidation of FFA initates an up-stream, chain-reaction-like inhibition of glycolytic enzymes, which ultimately inhibits glucose uptake. When considering the pronounced lipolytic effects of GH the Randle hypothesis remains an appealing model to explain the insulin-antagonistic effects of GH glucose metabolism. In support of this experiments have shown that co-administration of anti-lipolytic agents and GH reverses GH-induced insulin resistance. Similar conclusions were drawn from a recent study in GH deficient adults, which showed that insulin sensitivity was restored when acipimox (a nicotinic acid derivative) was co-administered with GH (41). It has, however, also been reported that GH-induced insulin resistance preceded the increase in circulating levels and forearm uptake of lipid intermediates (42). This early effect of GH on muscular glucose uptake could reflect intra-myocytic FFA release and oxidation and thus be compatible with the Randle hypothesis. It could also imply alternative (early) effects of GH. Moreover, the inhibitory effect of GH on muscle glycogen synthase activity (34) is not readily explained by substrate competition. According to the Randle hypothesis the fatty acid-induced insulin resistance will result in elevated intracellular levels of both glucose and glucose-6-phosphate. By contrast, muscle biopsies from GH deficient adults after GH treatment have revealed increased glucose but low-normal glucose-6-phosphate levels (43). Moreover, NMR spectroscopy studies in healthy adults indicate that FFA infusion results in a drop in the levels of both glucose and glucose-6-phosphate (44). The latter study did not involve GH administration, but it does challenge the Randle hypothesis and suggest that FFA may impair very early steps in glucose transporter activity (GLUT 4). The impact of GH on GLUT 4 translocation has not yet been studied in human subjects.

Implications For Gh Replacement

Regardless of the exact mechanisms, the insulin antagonistic effects may cause concern when replacing adult GH deficient patients with GH, since some of these patients are insulin resistant in the untreated state. There is evidence to suggest that the direct metabolic effects on GH may be balanced by long-term beneficial effects on body composition and physical fitness, but some studies report impaired insulin sensitivity in spite of favourable changes in body composition. There is little doubt that these effects of GH are dose-dependent and may be minimised or avoided if an appropriately low replacement dose is used. Still, the pharmacokinetics of s.c. GH administration is unable to mimick the endogenous GH pattern with suppressed levels after meals and elevations only during postabsorptive periods, such as during the night. This may be considered the natural domain of GH action which coincides with minimal beta-cell challenge. This reciprocal association between insulin and GH and its potential implications for normal substrate metabolism was initially recognised by Rabinowitz & Zierler (45) . The problems arise when GH levels are elevated during repeated prandial periods. The classic example is active acromegaly, but prolonged high dose s.c. GH administration may cause similar effects. Subcutaneous administration of GH in the evening probably remains the best compromise between effects and side effects (46), but it is far from physiological. We know and understand that hypoglycaemia is a serious and challenging side effect of insulin therapy as a consequence of inappropriately high insulin levels (during fasting). As a corollary, we must realise that hyperglycaemia may result from GH therapy. It is therefore important to carefully monitor glucose metabolism and to use the lowest effective dose when replacing adults with GH.

I've attached a diagram that shows, pretty simply, the interplay between various components of the endocrine system that are relevant here

awesome yet again. very informative.

"GH secretion is amplified during fasting and stress, whereas meals suppress GH release."
i remember reading somewhere that igf-1 levels are amplified post-prandial. if that is true, then how is gh amplified during fasting but not during meals? wouldn't a rise in gh coexist with a rise in igf-1? my memory might be incorrect though.

[einstein1905]

awesome yet again. very informative.

"GH secretion is amplified during fasting and stress, whereas meals suppress GH release."
i remember reading somewhere that igf-1 levels are amplified post-prandial. if that is true, then how is gh amplified during fasting but not during meals? wouldn't a rise in gh coexist with a rise in igf-1? my memory might be incorrect though.

Insulin levels increase post-prandial, which decreases the proteolytic enzymes that degrade IGFBPs, therefore IGF-1 levels are "stabilized", prevented, to a degree, from being degraded. IGF-1 directly acts as a negative feedback inhibitor of GH release via somatostatin/GHRH balance shift, hence meals suppressing GH release.
If you find where you saw IGF-1 levels increase in response to meals, which may be true, please post it.

Also, when they refer to GH supression, they are probably referring to less GH released per pulse rather than less frequent GH pulses. I want to do some more digging on that though.

[flexshack]

Insulin levels increase post-prandial, which decreases the proteolytic enzymes that degrade IGFBPs, therefore IGF-1 levels are "stabilized", prevented, to a degree, from being degraded. IGF-1 directly acts as a negative feedback inhibitor of GH release via somatostatin/GHRH balance shift, hence meals supressing GH release.
If you find where you saw IGF-1 levels increase in response to meals, which may be true, please post it.

Also, when they refer to GH supression, they are probably referring to less GH released per pulse rather than less frequent GH pulses. I want to do some more digging on that though.

i think "stabilized" is the word i saw to describe igf-1 levels as well. at least it rings a bell. i will keep looking though to see if i find anything different. thanks.

[BuffGuy]

You guys talking greek now.

But anyways, I talked to a doctor...and one who would actually tell me the truth..not one of those doctors who says everything is harmful and AS is the devil. He said that any raise in GH--be it exogenous or endogenous--can lead to diabetes in one pre-disposed. He says it is a common side-effect of GH.

[Ufa]

I had to edit this due to the fact that this thread is 2 years old..