Results 1 to 15 of 15
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09-05-2005, 02:44 PM #1
Roid gut from LR3 IGF1, IGF 1, IGF 2.
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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.
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09-05-2005, 03:43 PM #2
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....
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09-05-2005, 04:20 PM #3
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.
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09-05-2005, 07:03 PM #4Associate Member
- Join Date
- Jan 2005
- Posts
- 275
Originally Posted by Mr. Sparkle
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09-05-2005, 07:18 PM #5
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
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09-05-2005, 07:27 PM #6
sure, ask ronnie coleman
but pigs are big too (weight a lot) , you know?
(for the fanatics of lr3)
Originally Posted by oswaldosalcedoLast edited by oswaldosalcedo; 09-05-2005 at 07:37 PM.
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09-06-2005, 08:36 AM #7Originally Posted by Mr. Sparkle
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09-06-2005, 09:23 AM #8
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
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09-07-2005, 09:04 AM #9Associate Member
- Join Date
- Mar 2005
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- America
- Posts
- 353
fu#$kin lucky rats get it for free
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09-07-2005, 09:29 AM #10Originally Posted by HumanPerfection1
JohnnyB
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09-07-2005, 10:02 AM #11
you think those rats are like little ronnie coleman's with tails?
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09-08-2005, 07:16 PM #12Originally Posted by kingof516
of course, lol and big bellies too, lol......................
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09-08-2005, 09:21 PM #13
I'm a rat face that likes gear. Why do I have to pay for it?
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09-09-2005, 06:39 PM #14
.............
...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
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04-09-2018, 05:03 PM #15
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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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