By using IGF-1 will it make my brain release IGF-2?

[catlovesfood]

By using LR3 IGF-1 will my body release IGF-2 from my brain, pancreas etc? Im not looking for a GH gut..

[Seattle Junk]

Hehehe...I love cat's questions...There's no lying in his querys.....Yeah, actually I want to know this too.. I asked the same question a day or so ago.

[catlovesfood]

thanks SeattleJunk....................................bum p

[cubanojoe]

Johhny B can correct me if I am wrong, but I thought I seen a post from him on another form that he said;

Only HGH can and will be converted by the liver into IGF-1 and IGF-2.

R3IGF-1 does not convert at all to IGF-2 so you can not get GH gut from it, but you need to cycle it while HGH you do not.

[catlovesfood]

Johnny B......Where are you?!

[Seattle Junk]

Johhny B can correct me if I am wrong, but I thought I seen a post from him on another form that he said;

Only HGH can and will be converted by the liver into IGF-1 and IGF-2.

R3IGF-1 does not convert at all to IGF-2 so you can not get GH gut from it, but you need to cycle it while HGH you do not.

Johnny also mentioned that lr3 when used with anti inflamatories can cause igf-2 type sides or something to that nature.

[SPIKE]

Johnny also mentioned that lr3 when used with anti inflamatories can cause igf-2 type sides or something to that nature.

I think I'm becoming a AR forum junkie . Only b/c I remember both of those posts. Johnny is definitely the person to talk to about anything. Smart guy and helpful, I wish I had his knowledge . He's always one of the first if not to help others out.

[oswaldosalcedo]

imo, IGF 1 and IGF 2 bind and activate the IGF-1 receptor, The IGF-2 receptor only binds IGF-2 , it activates no intracellular signalling pathways, functioning only as an IGF-2 sequestering agent and preventing IGF-2 signalling.
that way IGF 1 dont bind to IGF 2 receptors, but gh gut is open question.
i will research.

[cubanojoe]

yes you are right. He said if you take an anti imflamatory all bets are off when using IFG-1 and gh gut.

[JohnnyB]

Johhny B can correct me if I am wrong, but I thought I seen a post from him on another form that he said;

Only HGH can and will be converted by the liver into IGF-1 and IGF-2.

R3IGF-1 does not convert at all to IGF-2 so you can not get GH gut from it, but you need to cycle it while HGH you do not.

Yes, IGF-II is released from the liver like IGF-1, so LR3 IGF-1 wouldn't convert to IGF-II. But I didn't read a study that showed LR3 IGF-1 with anti-infamitories can cause gut weight to increase. I'll get them and post those, remember, these are done on animals, so these are to be used as a possibility, not empirical evidence, since they're not done on humans, but for now there all we have.

JohnnyB

[JohnnyB]

Dexamethasone is an anti-inflamitory

Insulin-like growth factor-I (IGF-I) and especially IGF-I variants are anabolic in dexamethasone-treated rats.

Tomas FM, Knowles SE, Owens PC, Chandler CS, Francis GL, Read LC, Ballard FJ.

CSIRO Division of Human Nutrition, Adelaide, South Australia.

The administration of insulin -like growth factor-I (IGF-I) via subcutaneously implanted osmotic pumps partially reversed a catabolic state produced by the co-administration of 20 micrograms of dexamethasone/day to 150 g male rats. Marked dose-dependent effects on body weight and nitrogen retention were produced, with the highest IGF-I dose, 695 micrograms/day, giving a 6 g increase in body weight over 7 days, compared with a 19 g loss in the dexamethasone-only group and an 18 g gain in pair-fed controls. Two IGF-I analogues that bind poorly to IGF-binding proteins, the truncated form, des(1-3)IGF-I, and a variant with an N-terminal extension as well as arginine at residue 3, LR3IGF-I, were approx. 2.5-fold more potent than IGF-I. The response with LR3IGF-I was particularly striking because this peptide binds 3-fold less well than IGF-I to the type 1 IGF receptor. The increased potencies of the IGF-I variants may relate to the substantially increased plasma levels of IGF-binding proteins, particularly IGFBP-3, produced by the combined treatment of dexamethasone with IGF-I or the variants. These binding proteins would be expected to decrease the transfer of IGF-I, but not that of the variants, from blood to tissue sites of action. Measurements of muscle protein synthesis at the end of the treatment period and muscle protein breakdown by 3-methylhistidine (3MH) excretion throughout the experiment indicated coordinate anabolic effects of the IGF peptides on both processes. Thus 3MH excretion was decreased at the highest IGF-I dose from 83.5 +/- 4.2 (S.E.M.) mumol/kg per 7 days to 65.1 +/- 2.2, compared with 54.9 +/- 1.2 in the pair-fed controls. Part of this response in 3MH excretion may have reflected a decrease in gut protein breakdown, because IGF-I and especially the IGF analogues increased the gut weight by up to 45%. Notwithstanding the effects on protein synthesis and breakdown, the fractional carcass weights remained low in the IGF-treated groups, although the increase in total carcass weight reflected nitrogen rather than fat gain. The dexamethasone-induced changes in liver, spleen and heart weight were restored towards normal by the IGF treatment. The experiment demonstrates the potential of IGF-I treatment of catabolic states and especially the value of modified forms of growth factors that bind weakly to IGF-binding proteins.

JohnnyB

[JohnnyB]

The role of insulin-like growth factors in small intestinal cell growth and development.

MacDonald RS.

Nutritional Sciences Program, University of Missouri, Columbia, USA. [email protected]

IGF-I and IGF-II receptors are expressed in the small intestine of mammalian species, as are the genes to synthesize both peptides. IGF binding proteins are also expressed in the intestine. IGF-I and IGF-II mRNA are highest in fetal and newborn tissues and decrease with age. IGF-I mRNA is present in the adult small intestine, and is associated with the submucosal regions and crypt cells. IGF-I and IGF-II receptor binding to the small intestine is higher in newborn animals and decreases with age. Both receptors are more concentrated in the crypt than villus regions, but IGF-II binding is higher than IGF-I in all regions. IGF-I receptors are associated with the submucosal region of the small intestine, whereas IGF-II receptors are more abundant in the mucosal cells. Administration of IGF-I either orally or by osmotic pump generally has no affect on small intestinal weight or length, but does increase mucosal cellularity. LR3-IGF-I administration by osmotic pump affects the small intestine similarly to IGF-I, although with a higher potency. In the few studies in which IGF-II was administered, increased gut mass was observed in adult rats, but not newborn rats or pigs. Significant effects on mucosal expression of disaccharidases was achieved with either oral or subcutaneous IGF-I or oral IGF-II. Administration of IGF in models of intestinal hypertrophy and atrophy are also reviewed.

JohnnyB

[Seattle Junk]

The role of insulin-like growth factors in small intestinal cell growth and development.

MacDonald RS.

Nutritional Sciences Program, University of Missouri, Columbia, USA. [email protected]

IGF-I and IGF-II receptors are expressed in the small intestine of mammalian species, as are the genes to synthesize both peptides. IGF binding proteins are also expressed in the intestine. IGF-I and IGF-II mRNA are highest in fetal and newborn tissues and decrease with age. IGF-I mRNA is present in the adult small intestine, and is associated with the submucosal regions and crypt cells. IGF-I and IGF-II receptor binding to the small intestine is higher in newborn animals and decreases with age. Both receptors are more concentrated in the crypt than villus regions, but IGF-II binding is higher than IGF-I in all regions. IGF-I receptors are associated with the submucosal region of the small intestine, whereas IGF-II receptors are more abundant in the mucosal cells. Administration of IGF-I either orally or by osmotic pump generally has no affect on small intestinal weight or length, but does increase mucosal cellularity. LR3-IGF-I administration by osmotic pump affects the small intestine similarly to IGF-I, although with a higher potency. In the few studies in which IGF-II was administered, increased gut mass was observed in adult rats, but not newborn rats or pigs. Significant effects on mucosal expression of disaccharidases was achieved with either oral or subcutaneous IGF-I or oral IGF-II. Administration of IGF in models of intestinal hypertrophy and atrophy are also reviewed.

JohnnyB

So what does that mean? Does that mean lr3 can cause growth like IGF-2 or that the small intestines increase in mucosal cellularity. What is mucosal cellularity? I'm guessing the ability to absorb nutrients? Doesn't it take IGF-2 to make them grow in size?

The questions is, does lr3 IGF-1 have the potential to give you roid gut, small intenstinal growth?

[cubanojoe]

I would say NO, but that is only my option.

[Seattle Junk]

I would say NO, but that is only my option.

You must know my gf?

[IBdmfkr]

I believe it will with prolonged use or abused dosages. We really don't know, there are not any studies on humans to my knowledge.

[cubanojoe]

true, but everyone says the main cause for growth in the gut and bones is IGF-2. Only HGH converts into both , not sure how IGF-1 could be converted into IGF-2

[Seattle Junk]

true, but everyone says the main cause for growth in the gut and bones is IGF-2. Only HGH converts into both , not sure how IGF-1 could be converted into IGF-2

High amounts of GH may cause roid gut. We're talking 10ius+ ed. Probably more like 15ius+ to see adverse effects. Diminishing returns at the higher amounts anyway. Just a waste of money with a huge gut at the price of a used luxury car. What's your estimate (GH - ius/day) Johnny or Pinnacle when roid gut gets in your belly?

[oswaldosalcedo]

anyone produces it (IGF 1/IGF 2).

see:
Am J Physiol Gastrointest Liver Physiol 266: G1090-G1098
Prolonged administration of IGF peptides enhances growth of gastrointestinal tissues in normal rats

C. B. Steeb, J. F. Trahair, F. M. Tomas and L. C. Read
Cooperative Research Center for Tissue Growth and Repair, North Adelaide, South Australia.

To investigate the effect of insulin -like growth factor (IGF) peptide infusion on the gastrointestinal tract, female rats (115 g, 6/group) were treated for 14 days with IGF-I or long R (LR3IGF-I; 0, 44, 111, or 278 micrograms/day) delivered by osmotic minipumps. Both peptides induced a dose-dependent increase in gastrointestinal tissue weight. Total gut weight, small intestinal weight, and small intestinal length increased by 43, 47, and 13%, respectively, after treatment with 278 micrograms/day of LR3IGF-I. Crypt depth and villus height increased after peptide treatment with an associated increased crypt cell population (+33%), cells per villus column (+34%), and villus cell density (+20%). Proportional increments in proliferating cell nuclear antigen labeling and an unaltered crypt growth fraction indicated that the balance between the proliferative and maturation compartment of the crypt was maintained. Fecal nitrogen excretion was significantly reduced in rats treated with LR3IGF-I, suggesting an increased absorptive capacity of the duodenum. The enhanced potency of LR3IGF-I supports previous findings that the gut is especially responsive to analogues with reduced binding affinity to IGF-binding proteins.



see:
Am J Physiol. 1997 Mar;272
Systemic infusion of IGF-I or LR(3)IGF-I stimulates visceral organ growth and proliferation of gut tissues in suckling rats.

Steeb CB, Shoubridge CA, Tivey DR, Read LC.

Child Health Research Institute and Cooperative Research Center for Tissue Growth and Repair, North Adelaide, South Australia.

This study describes developmental changes in gastrointestinal response to insulin-like growth factor I (IGF-I) peptide administration. Neonatal rats were infused with IGF-I or long [Arg3]IGF-I (LR(3)IGF-I) for 6.5 days starting on day 6 or 12 postpartum. Peptides were delivered by mini osmotic pumps at 0, 2, 5, or 12.5 microg x g(-1) x day(-1). IGF-I infusion increased plasma IGF-I levels in both age groups but stimulated body weight gain only in the older rats. Infusion of LR(3)IGF-I did not change plasma IGF-I levels. Both peptides enhanced expression of IGF-binding proteins (IGFBP) 1 and 2 and induced IGFBP-3 in the older rats. For both age groups, weights of the kidney and spleen increased by up to 85 and 76%, respectively. IGF-I treatment also stimulated gut weight and length by up to 60 and 32%, respectively, but dose dependency was observed only in the older rats. LR(3)IGF-I was more potent for all growth parameters in both age groups. Histological observations included thickening of the mucosa and muscularis externa after infusion of IGF-I peptides. Thymidine labeling in the younger rats indicated that proliferative activity increased proportionately with crypt cell growth. These results show that IGF-I peptides selectively stimulate growth of gastrointestinal tissues in suckling rats and that the proximal gut was the most peptide-responsive region.

Journal of Endocrinology, Vol 144, Issue 1, 91-98
Copyright © 1995 by Society for Endocrinology
Continuous 14 day infusion of IGF-II increases the growth of normal female rats, but exhibits a lower potency than IGF-I
MA Conlon, GL Francis, FM Tomas, JC Wallace, GS Howarth, and FJ Ballard



The effects of continuous 14 day infusion of recombinant human IGF-I (104 or 260 micrograms/day) or IGF-II (104, 260 or 650 micrograms/day) via s.c. implanted osmotic pumps were compared in young female rats in order to establish the relative efficacies of these two growth factors. Significant increase in body weight gain and feed conversion efficiency were achieved by 260 micrograms/day of IGF-I or 650 micrograms/day of IGF-II. These treatments were associated with increased nitrogen retention and increases in the fractional weights of kidneys, spleen, total gut and individual gut regions. There was an increase in the size of villi and muscularis lining the jejunum, suggesting an increased absorptive capacity of the gut. However there was no significant change in the amount of faecal nitrogen excretion when expressed as a percentage of nitrogen intake. Interestingly, IGF-II was at least as potent as IGF-I in increasing the depth of jejunal crypts. Infusion of equivalent doses of either IGF-I or IGF-II resulted in similar increases in circulating concentrations of the respective peptides, though IGF-II infusion dose-dependently decreased plasma IGF-I concentrations from those of the controls. Plasma IGF-binding protein levels were increased by both IGF-I and IGF-II treatments, though IGF-I elicited greater responses. In summary, IGF-II can promote the growth of young female rats, although generally less potently than IGF-I.

see:
J Endocrinol. 1995 Aug;146(2):247-53. Related Articles, Links


Long R3 insulin-like growth factor-I (IGF-I) infusion stimulates organ growth but reduces plasma IGF-I, IGF-II and IGF binding protein concentrations in the guinea pig.

Conlon MA, Tomas FM, Owens PC, Wallace JC, Howarth GS, Ballard FJ.

Department of Biochemistry, University of Adelaide, Australia.

We have tested whether an animal with substantial amounts of both IGF-I and IGF-II in circulation, such as the guinea pig, would respond to chronic IGF infusion in the same manner as the adult rat, which has negligible amounts of IGF-II in blood. Female guinea pigs of 350 g body weight were continuously infused for 7 days with recombinant guinea pig IGF-I or -II (120 or 360 micrograms/day) or long R3 IGF-I (LR3IGF-I) (120 micrograms/day), an analogue which has much reduced affinities for IGF binding proteins. IGF-I or IGF-II infusion led to substantial increases in plasma IGF-I or IGF-II respectively in comparison with vehicle-infused animals. Nevertheless, body weight gain, feed intake, feed conversion efficiency and carcass composition were not significantly affected by any treatment (significance was deemed to be P < 0.05). Amongst the tissues examined only the fractional weight (g/kg body weight) of the adrenals was increased, and that only by the higher dose (360 micrograms/day) of IGF-I. However, the fractional weight of adrenals, gut, kidneys and spleen were significantly increased by LR3IGF-I, but again overall growth was not stimulated. A possible explanation for the lack of IGF-I effects is that total circulating IGF concentrations were not increased by these treatments. IGF-II significantly raised total IGF concentrations at the higher dose only. Plasma IGF-I was reduced by IGF-II infusion, as was plasma IGF-II by IGF-I infusion

[catlovesfood]

so is that a yes or a no? or is it both - like if you use high amounts you can get it, but if the dose is low you cant? opinions?

[oswaldosalcedo]

I think that 50 mcg daily (1-2 months) would not kill anybody.

but I might not assure it in a conclusive way.

[powerliftmike]

this is interesting stuff i wanted to bump this thread back up. So is the main culprit of gut growth IGF-II?

[powerliftmike]

bump for oswaldosalcedo and JohnnyB. Or anybody else that may know.

[oswaldosalcedo]

any igf I, II, LR3, can cause gut growth at certain doses.