igf-1 LR3 questions

im just wondering about the stuff already mixed in BA... does it come in a vial which can be repunctured by pins (like vials of test or vials of deca)... or does it have to be mixed with something?

plus with igf-1 lr3 will 40mcg/day (for 4 weeks) be sufficient to make gains for a first time user? ive heard you need higher dosages for results but im just using this for a hardening effect during PCT to keep all my gains, not really to add any extra muscle on (ofcourse it would be nice, but i need to save my cash)

oh and is it IGF-1 or HGH that causes the "growth gut" that everyone talks about it?

it comes in a vial witha rubber stopper like aas

ya 40mcg is a good dose for 1st time

gh will casue organ growth if abused over a long period of time ata very high dose, i also read a study that said igf mixed w/ anti-inflamatories might cause organ growth.

do you have to refridgerate it?

and whats the diff between media grade and receptor grade?

bump

Quote:

---

Originally Posted by tycin

it comes in a vial witha rubber stopper like aas

ya 40mcg is a good dose for 1st time

gh will casue organ growth if abused over a long period of time ata very high dose, i also read a study that said igf mixed w/ anti-inflamatories might cause organ growth.

---

Hey Tycin, that is very interesting about the IGF and anti inflamatories, do you have that study by chance? I've never heard that before and would like to learn more about it......

Quote:

---

Originally Posted by tycin

it comes in a vial witha rubber stopper like aas

ya 40mcg is a good dose for 1st time

gh will casue organ growth if abused over a long period of time ata very high dose, i also read a study that said igf mixed w/ anti-inflamatories might cause organ growth.

---

HGH can cause it because it also elevates IGF-II, Here's the study on LR3 and small intestine


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

Quote:

---

Originally Posted by c5529

Hey Tycin, that is very interesting about the IGF and anti inflamatories, do you have that study by chance? I've never heard that before and would like to learn more about it......

---

Here it is
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

should it be refridgerated?
and whats the difference between media and receptor grade?

Quote:

---

Originally Posted by jgg1221

should it be refridgerated?
and whats the difference between media and receptor grade?

---

if it is in BA it should be stored in the freezer