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  1. #1
    oswaldosalcedo's Avatar
    oswaldosalcedo is offline Senior Member
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    Roid gut from LR3 IGF1, IGF 1, IGF 2.

    .

    Roid gut from LR3 IGF1, IGF 1, IGF 2.

    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. "

    There are some studies done in pigs too.
    Last edited by oswaldosalcedo; 09-05-2005 at 02:59 PM.

  2. #2
    Mr. Sparkle's Avatar
    Mr. Sparkle is offline Slinabolic Vet / Retired
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    278 mcg would make your gut grow for sure.... but remember these rats are small. So to say that 44mcg would make your gut grow isnt totally true...
    how much does a rat weigh? a pound or two?
    So seems the same ratio is a GRAM of IGF for a human...

    IMO dont worry about it....

  3. #3
    Nicky B's Avatar
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    The only thing I would worry about is I mistakenly got igf-2. But I never even seen or heard of someone buying igf-2.

  4. #4
    Slic4788 is offline Associate Member
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    Quote Originally Posted by Mr. Sparkle
    278 mcg would make your gut grow for sure.... but remember these rats are small. So to say that 44mcg would make your gut grow isnt totally true...
    how much does a rat weigh? a pound or two?
    So seems the same ratio is a GRAM of IGF for a human...

    IMO dont worry about it....
    i concur...

  5. #5
    kingof516's Avatar
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    well i feel like i have a gut from this round of igf...im two and a half weeks in, and my stomach looks beyond bloated

  6. #6
    oswaldosalcedo's Avatar
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    sure, ask ronnie coleman
    but pigs are big too (weight a lot) , you know?
    (for the fanatics of lr3)

    Quote Originally Posted by oswaldosalcedo
    .

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

    ................(LR3IGF-I; 0, 44, 111, or 278 micrograms/day) ...............
    43, 47, and 13%....................................

    and:
    There are studies done in pigs too.
    Last edited by oswaldosalcedo; 09-05-2005 at 07:37 PM.

  7. #7
    Seattle Junk's Avatar
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    Quote Originally Posted by Mr. Sparkle
    278 mcg would make your gut grow for sure.... but remember these rats are small. So to say that 44mcg would make your gut grow isnt totally true...
    how much does a rat weigh? a pound or two?
    So seems the same ratio is a GRAM of IGF for a human...

    IMO dont worry about it....
    So a 1lb rat at 278mcgs would = 200lb human at 55,600mcgs or 55.6 grams. Yeah, ok. Like somebody is going to shoot that much lr3 IGF-1. Sure, it'll give you gut growth along with a lot of other things growing out of control. That amount doesn't even make sense so how can it be a real study?

  8. #8
    JohnnyB's Avatar
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    Here's one that cancels out the one posted. We need to remember that all studies on LR3 IGF-1, are done on animals, none are done on humans that I can find or have access too. So they're good for info reasond but to get a definitive answer, it's not going to happen.

    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

  9. #9
    HumanPerfection1 is offline Associate Member
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    fu#$kin lucky rats get it for free

  10. #10
    JohnnyB's Avatar
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    Quote Originally Posted by HumanPerfection1
    fu#$kin lucky rats get it for free


    JohnnyB

  11. #11
    kingof516's Avatar
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    you think those rats are like little ronnie coleman's with tails?

  12. #12
    oswaldosalcedo's Avatar
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    Quote Originally Posted by kingof516
    you think those rats are like little ronnie coleman's with tails?

    of course, lol and big bellies too, lol......................

  13. #13
    Seattle Junk's Avatar
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    I'm a rat face that likes gear. Why do I have to pay for it?

  14. #14
    oswaldosalcedo's Avatar
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    .............
    ...sheeps also get their bellies, for free !


    BODY GROWTH, CARCASS COMPOSITION, AND ENDOCRINE
    CHANGES IN LAMBS CHRONICALLY TREATED WITH
    RECOMBINANTLY DERIVED INSULIN-LIKE GROWTH FACTOR-1


    YVETTE H. COTTAM, HUGH T. BLAIR, BRIAN W. GALLAHER,
    ROGER W. PURCHAS, BERNHARD H. BREIER, STUART N. MCCUTCHEON, AND PETER D. GLUCKMAN


    male sheeps were treated for 8 weeks with either 50 mcg/kg body wt/8 hourly SC insulin -like growth factor-I (IGF-I) (n = 10) or with saline (n = 9). IGF-I treatment increased plasma IGF-I from 235 + 17 to 347 + 16 rig/ml (P < 0.001).

    suggesting that in the well fed animal with an intact somatotropic
    axis IGF-I treatment at doses which double plasma IGFI
    does not enhance somatic growth performance. However, the
    marked splenomegaly shows the sensitivity of splenic growth to
    systemic IGF-I.
    The suppression of insulin with chronic IGF-I
    treatment was accompanied by hyperglycaemia-this may explain
    in part the lack of a significant anabolic response and may
    limit the utility of IGF-I therapy unless higher doses with
    insulin-like effects are used. (Endocrinology 130: 2924-2930)….

    …..In conclusion, exogenous IGF-I administered at physiological
    doses did not exert marked effects on body wt
    gain, carcass dimensions, or body composition in intact,
    growing, and well-fed yearling sheep. It had some marked
    endocrine and metabolic effects, however, including
    suppression of plasma insulin, IGFBP-2, and induced
    hyperglycaemia. Marked splenomegaly was also noted.
    These changes must be borne in mind in considering any
    possible therapeutic use of IGF-I. While IGF-I treatment
    in this study did not cause a major somatogenic response
    in well fed normally growing animals, higher doses of
    IGF-I may be more effective. However, under more severe
    conditions such as undernutrition, when GH resistance
    occurs (44) IGF-I is a more effective anabolic agonist…..

    Organ- control- igf 1 treated

    Heart 232.0 +/- 11.0 ------- 230.4 +/ 10.4
    Liver 1005.9 +/- 48.5 ----- 1027.0 +/- 45.9
    Spleen 78.8 +/- 4.6 ------ 114.6 +/- 4.4 (50 %)
    Lungs 502.6 +/- 29.9 ------ 515.1+/- 28.3
    Kidneys 131.8 +/- 5.3 ------ 145.6 +/- 5.0

  15. #15
    oswaldosalcedo's Avatar
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    .

    Stimulation of intestinal growth is associated with increased insulin-like growth factor-binding protein 5 mRNA in the jejunal mucosa of insulin-like growth factor-I-treated parenterally fed rats



    https://www.ncbi.nlm.nih.gov/pubmed/9402151

    Surgically stressed rats maintained with total parenteral nutrition (TPN) exhibit jejunal atrophy, which can be attenuated by insulin -like growth factor-I (IGF-I) but not by growth hormone (GH) treatment. In order to understand the basis for the selective action of IGF-I, the levels of mRNAs encoding IGF-I, IGF-binding proteins (IGFBPs), IGF-I receptor, and GH receptor/binding protein (GHR/GHBP) were determined in rats given TPN and treated with GH, IGF-I, or GH + IGF-I. GH treatment significantly stimulated hepatic IGF-I mRNA. IGF-I treatment did not alter liver IGF-I mRNA, nor was there any evidence for interaction between GH and IGF-I. Jejunal mucosa IGF-I mRNA was extremely low and was not altered by TPN or by any of the hormonal treatments. The inability of GH to stimulate jejunal growth was not associated with a deficiency in GHR/GHBP mRNA. In jejunal mucosa, IGF-I and GH treatment independently and synergistically stimulated IGFBP-3 mRNA. IGF-I stimulated jejunal IGFBP-5 mRNA, but GH had no effect on IGFBP-5 mRNA. The levels of IGF-I receptor and IGFBP-1, 2, 4, and 6 mRNAs were extremely low and/or were not altered by any of the treatments.
    These results suggest that the ability of exogenous IGF-I,
    but not GH, to induce IGFBP-5 mRNA in jejunal mucosa may lead to the selective growth-promoting effect of IGF-I. Jejunal mucosa IGFBP-3 mRNA levels were not correlated with altered growth. We postulate that IGFBP-5 positively modulates the anabolic effects induced by exogenous IGF-I in the jejunum.


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