I have to disagree here. There are actually 3 well defined feedback mechanisms for GH production and they all work on different intervals (ie ultrashort loop, short loop and long loop) and they have varying effects effects on the pulsitile nature of GH release. Its a very common misconception, but over the past couple years there have been great advancements in identifying the GH-IGF-1 axis.XXXL said:yup, just a money thing. if you can, go 7 on and 0 off.
unlike test, gh injections won't suppress you natual gh production. after a couple hours your body is able to beging production again.
My pleasurenautica said:Thanks zyg,
Once again you have confusted the hell out of me.![]()
Nautica
Zyglamail said:My pleasure
Im a bit short on time at themoment but if I can get to my comp later tonight I will try and elaborate on the methods of feedback so this becomes a bit more clear.
Actually the long term effects are much longer than a couple hours. Here is just one abstract.XXXL said:yes, that is a new one to me. i'd love for you to post the info and where it came from. maybe some links.
and how long are the intervals? (ultrashort,short, and long) is the longest one less than 2 hours? if that is the case, i don't see what you'r saying.
post the info, it would be a great read.
thanks!
J Clin Endocrinol Metab 2001 Apr;86(4):1731-7 Related Articles, Books, LinkOut
Changes in non-22-kilodalton (kDa) isoforms of growth hormone (GH) after administration of 22-kDa recombinant human GH in trained adult males.
Wallace JD, Cuneo RC, Bidlingmaier M, Lundberg PA, Carlsson L, Boguszewski CL, Hay J, Boroujerdi M, Cittadini A, Dall R, Rosen T, Strasburger CJ.
Metabolic Research Unit, Department of Medicine, University of Queensland, Princess Alexandra Hospital, Brisbane 4102, Australia. [email protected]
GH is being used by elite athletes to enhance sporting performance. To examine the hypothesis that exogenous 22-kDa recombinant human GH (rhGH) administration could be detected through suppression of non-22-kDa isoforms of GH, we studied seventeen aerobically trained males (age, 26.9 +/- 1.5 yr) randomized to rhGH or placebo treatment (0.15 IU/kg/day for 1 week). Subjects were studied at rest and in response to exercise (cycle-ergometry at 65% of maximal work capacity for 20 min). Serum was assayed for total GH (Pharmacia IRMA and pituitary GH), 22-kDa GH (2 different 2-site monoclonal immunoassays), non-22-kDa GH (22-kDa GH-exclusion assay), 20-kDa GH, and immunofunctional GH. In the study, 3 h after the last dose of rhGH, total and 22-kDa GH concentrations were elevated, reflecting exogenous 22-kDa GH. Non-22-kDa and 20-kDa GH levels were suppressed. Regression of non-22-kDa or 20-kDa GH against total or 22-kDa GH produced clear separation of treatment groups. In identical exercise studies repeated between 24 and 96 h after cessation of treatment, the magnitude of the responses of all GH isoforms was suppressed (P < 0.01), but the relative proportions were similar to those before treatment. We conclude: 1) supraphysiological doses of rhGH in trained adult males suppressed exercise-stimulated endogenous circulating isoforms of GH for up to 4 days; 2) the clearest separation of treatment groups required the simultaneous presence of high exogenous 22-kDa GH and suppressed 20-kDa or non-22-kDa GH concentrations; and 3) these methods may prove useful in detecting rhGH abuse in athletes.
Insulin-like growth factor I action on rat anterior pituitary cells: suppression of growth hormone secretion and messenger ribonucleic acid levels
S Yamashita and S Melmed
Somatomedin preparations have previously been shown to suppress GH release. The effects of a synthetic recombinant human insulin-like growth factor analog (IGF-I; Thr 59) were, therefore, tested on long term GH secretion by male rat pituitary monolayer cell cultures grown in serum-free defined medium. IGF-I (3.25 nM) maximally suppressed basal GH secretion for up to 72 h by 66%, with an ED50 of 0.1 nM. Human pancreatic GRF-(1-44) (GHRH; 1 nM) stimulated GH secretion by 230% during 72 h. IGF-I (0.13 nM) suppressed GHRH-stimulated GH secretion by 30% (P less than 0.005). IGF-I (0.625 nM) completely abolished stimulation of GH by GHRH (1 nM), while higher doses of IGF-I (up to 6.5 nM) actually suppressed GH secretion even in the presence of GHRH (up to 1 nM). The depletion of intracellular GH levels in GHRH-treated cells was reversed by IGF-I (3.25 nM). PRL secretion was not altered in the same cells by IGF-I. Equivalent doses of epidermal growth factor and fibroblast growth factor did not alter basal or GHRH-stimulated GH secretion. Nitrocellulose dot hybridization of immobilized pituitary cell RNA extracts with rat GH [32P]cDNA showed that cellular GH mRNA levels were lowered in IGF-I-treated cells in a dose-dependent manner. Maximal suppression of GH mRNA was achieved with 0.65 nM IGF-I. IGF-I also inhibited the 3-fold stimulation of GH mRNA induced by 1 nM GHRH. The data show that IGF-I directly modulates GH gene expression at the level of the somatotroph by inhibiting basal and GHRH-stimulated GH secretion and GH mRNA levels during 72 h. These effects may occur at different postranscriptional sites. Alternatively, they may result from a direct inhibition of IGF-I on GH gene transcription.
The growth hormone (GH)-releasing hormone (GHRH)-GH-somatomedin axis: evidence for rapid inhibition of GHRH-elicited GH release by insulin- like growth factors I and II
GP Ceda, RG Davis, RG Rosenfeld and AR Hoffman
Hypothalamic-pituitary-end-organ axes are frequently controlled by long loop negative feedback homeostatic mechanisms. Insulin-like growth factor I (IGF-I), IGF-II, and insulin receptors have recently been described in normal and neoplastic rat and acromegalic human pituitary cells, a finding which suggests the possibility that somatomedins might exert feedback at the level of the anterior pituitary. To study the kinetics of this feedback response, we used perifused dispersed rat anterior pituitary cells to learn if somatomedins or insulin could inhibit GH-releasing hormone (GHRH)-stimulated GH secretion. Cells were exposed to hourly boluses of 1 nM GHRH with or without varying doses of IGF or insulin. IGF-I inhibited GHRH-elicited GH release with an IC50 of 6.5 nM; maximal inhibition (approximately 67%) was achieved with 10 nM IGF-I. IGF-II was a less potent hormone, with 10 nM inhibiting about 30% of GHRH-stimulated GH release. Slight inhibition of stimulated GH release (less than 15%) was seen when cells were treated with insulin, but only when doses of insulin of 10 nM or more were used. In conclusion, nanomolar concentrations of IGF-I and IGF-II inhibited GHRH- elicited GH release from perifused rat pituitary cells in a dose- dependent manner; and insulin was not an effective inhibitor of stimulated GH release at physiological peptide concentrations. In conjunction with our previous findings that the concentrations of IGF-I and IGF-II receptors greatly exceed that of insulin receptors on normal rat pituitary cells, we hypothesize that the GH-inhibiting action of high dose insulin is mediated through an IGF receptor.
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