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  1. #1
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    Exogenous GH and its effects on endogenous GH

    For all of you that assume I just ramble without justification of what I say, I refer to you as the silent majority, I found a study that actually just about exactly shows what I've been saying about exogenous GH's effects on endogenous GH production/release. I've always postulated that taking exogenous GH should suppress 1 maybe two endogenous GH pulses, based on the half life of GH itself, not really significant, and also based on the half-life of IGF-1, which can vary quite a bit depending on IGFBPs. GH pulses occur about every 2-3 hours, but that interval can also vary.
    Here's a study that proves I'm not retarded:

    Lanzi R, Tannenbaum GS. Journal of Endocrinology

    Department of Pediatrics, McGill University, Montreal, Quebec, Canada.

    Endogenous pulsatile GH secretion is blunted by the administration of exogenous GH; however, few data are available on the time course of GH negative feedback, and the mechanism by which this occurs still remains unclear. In the present study, we examined the temporal pattern of the inhibitory effect induced by an acute (single) and chronic (5 days) sc recombinant human (rh) GH injection regimen on spontaneous GH release in the rat and assessed the possible involvement of the hypothalamic GH-inhibitory peptide, somatostatin (SRIF), in this response. Eight-hour (0800-1600 h) GH secretory profiles, obtained from free-moving adult male rats administered a single sc injection of 200 micrograms rhGH at 0800 h, revealed a marked suppression of spontaneous GH pulses (GH peak amplitude: 45.7 +/- 10.9 vs. 207.8 +/- 31.7 ng/ml in H2O-injected control rats; P less than 0.001) lasting for up to 4.1 +/- 0.1 h after the injection (mean 4-h plasma GH level: 13.6 +/- 3.6 vs. 49.4 +/- 7.0 ng/ml in H2O-injected controls; P less than 0.01). During the subsequent 4- to 8-h period, recovery of spontaneous GH secretory bursts was evident, and neither the GH peak amplitude nor mean 4-h plasma GH level of rhGH-treated rats was significantly different from that of H2O-injected controls. The magnitude, time course, and recovery of the rhGH-induced inhibitory effect on pulsatile GH release after chronic rhGH treatment was similar to that after a single injection. Passive immunization of rhGH-treated rats with SRIF antiserum reversed the rhGH-induced inhibition of spontaneous GH pulses (peak amplitude: 131.7 +/- 53.7 vs. 7.1 +/- 3.4 ng/ml in rhGH-treated control rats given normal sheep serum; P less than 0.05) and restored both the GH peak amplitude and mean plasma GH level to values similar to those in H2O-injected controls. Taken together, these results demonstrate that: 1) the inhibitory effect of rhGH on endogenous pulsatile GH release is of short duration (approximately 4 h); 2) the time course of this response does not change after 5-day repeated rhGH administration; and 3) the feedback effect of GH on its own spontaneous release is exerted, at least in part, by increasing hypothalamic SRIF secretion. Such a mechanism of GH feedback may be important in the physiological control of pulsatile GH secretion.

  2. #2
    flexshack is offline Member
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    Quote Originally Posted by einstein1905
    For all of you that assume I just ramble without justification of what I say, I refer to you as the silent majority, I found a study that actually just about exactly shows what I've been saying about exogenous GH's effects on endogenous GH production/release. I've always postulated that taking exogenous GH should supress 1 maybe two endogenous GH pulses, based on the half life of GH itself, not really significant, and also based on the half-life of IGF-1, which can vary quite a bit depending on IGFBPs. GH pulses occur about every 2-3 hours, but that interval can also vary.
    Here's a study that proves I'm not retarded:

    Lanzi R, Tannenbaum GS. Journal of Endocrinology

    Department of Pediatrics, McGill University, Montreal, Quebec, Canada.

    Endogenous pulsatile GH secretion is blunted by the administration of exogenous GH; however, few data are available on the time course of GH negative feedback, and the mechanism by which this occurs still remains unclear. In the present study, we examined the temporal pattern of the inhibitory effect induced by an acute (single) and chronic (5 days) sc recombinant human (rh) GH injection regimen on spontaneous GH release in the rat and assessed the possible involvement of the hypothalamic GH-inhibitory peptide, somatostatin (SRIF), in this response. Eight-hour (0800-1600 h) GH secretory profiles, obtained from free-moving adult male rats administered a single sc injection of 200 micrograms rhGH at 0800 h, revealed a marked suppression of spontaneous GH pulses (GH peak amplitude: 45.7 +/- 10.9 vs. 207.8 +/- 31.7 ng/ml in H2O-injected control rats; P less than 0.001) lasting for up to 4.1 +/- 0.1 h after the injection (mean 4-h plasma GH level: 13.6 +/- 3.6 vs. 49.4 +/- 7.0 ng/ml in H2O-injected controls; P less than 0.01). During the subsequent 4- to 8-h period, recovery of spontaneous GH secretory bursts was evident, and neither the GH peak amplitude nor mean 4-h plasma GH level of rhGH-treated rats was significantly different from that of H2O-injected controls. The magnitude, time course, and recovery of the rhGH-induced inhibitory effect on pulsatile GH release after chronic rhGH treatment was similar to that after a single injection. Passive immunization of rhGH-treated rats with SRIF antiserum reversed the rhGH-induced inhibition of spontaneous GH pulses (peak amplitude: 131.7 +/- 53.7 vs. 7.1 +/- 3.4 ng/ml in rhGH-treated control rats given normal sheep serum; P less than 0.05) and restored both the GH peak amplitude and mean plasma GH level to values similar to those in H2O-injected controls. Taken together, these results demonstrate that: 1) the inhibitory effect of rhGH on endogenous pulsatile GH release is of short duration (approximately 4 h); 2) the time course of this response does not change after 5-day repeated rhGH administration; and 3) the feedback effect of GH on its own spontaneous release is exerted, at least in part, by increasing hypothalamic SRIF secretion. Such a mechanism of GH feedback may be important in the physiological control of pulsatile GH secretion.

    okay, i believe you now. you are not retarded.
    lol, good study. thanks.

  3. #3
    KGBnine is offline Anabolic Member
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    another good read by einstein. Keep up the good work bro.

  4. #4
    BuffGuy is offline Associate Member
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    Einstein, I don't think you even need to defend yourself. Your posts have been EXTREMELY beneficial to me, and were helpful in the hours of research I have put in as I plan on taking the plunge soon...

    It's guys like you that make this website so awesome and beneficial to newbies (and I guess veterans too, although I can't speak for them)...

  5. #5
    Solrock's Avatar
    Solrock is offline Member
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    Feeling the need to prove you are not retarded Einstein... now that's funny. I can't imagine anyone on this baord or another thinking of you as retarded.

    Once again, great post.

  6. #6
    flexshack is offline Member
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    Quote Originally Posted by Solrock
    Feeling the need to prove you are not retarded Einstein... now that's funny. I can't imagine anyone on this baord or another thinking of you as retarded.

    Once again, great post.
    speak for yourself. i have always had my doubts. i mean just look at his avatar. JUST KIDDING, LOL.
    einstein is THE MAN in my book.

  7. #7
    jbigdog69's Avatar
    jbigdog69 is offline Banned
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    Yea this is insane for Einstein to have to defend himself. Those who oppose step forward and be a man. We will track you down and hang you by your toes and let the blood drip from the small incisions we have made across your forehead...oops...got to stop watching the new Matrix Movie. lol

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