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  1. #1
    Mallet's Avatar
    Mallet is offline Anabolic Member
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    Local effects of GH

    DIRECT LOCAL EFFECTS OF GH/TNF-α ON IGF-I/INSULIN SENSITIVITY IN SKELETAL MUSCLE
    CE Stewart, X He, JM Holly. Surgery, Uni. of Bristol, Bristol, United Kingdom

    Type 2 diabetes/beta cell failure affects 140 million people worldwide. The diabetogenic effects of growth hormone (GH) are well established, and GH hypersecretion has been implicated in the aetiology of insulin resistance in catabolic conditions. Increasing evidence implicates other cytokines, e.g. TNFα, in these insulin-resistant states. The net effects of increased circulating/local cytokine concentrations in diabetes need to be clarified. Since skeletal muscle is a major target tissue of insulin action, we used murine C2 cell lines and primary human myoblast cultures to investigate the relationship between local GH/TNFα and IGF/insulin signalling. We have previously shown that TNFα blocks differentiation and induces apoptosis in C2 cells, following suppression of IGF-II and IGFBP-5 secretion. We have since established that GH (20 ng/ml) does not alter differentiation or apoptosis relative to controls. IGF-I (100 ng/ml), which alone caused a 25 % reduction in differentiation was not affected by a co-incubation with GH. Immunoblotting demonstrated that while GH was without effect on IGFBP-5 secretion, it increased levels induced by IGF-I, and enhanced IGF-induced MAP kinase activation, suggesting that GH may facilitate a pro-mitogenic role of IGF-I in muscle. In our primary adult human myotubes, we have found that insulin promotes a dose responsive glucose uptake compared with controls (142▒15% (1ÁIU/ml), 198▒35% (30 ÁIU/ml), p<0.01). We have also found that TNFα (20 ng/ml), or GH (both of which are elevated in diabetes) suppress basal glucose uptake compared with controls (to 63% and 26.9% vs 100 %, respectively). Insulin stimulated glucose uptake (1 and 30 ÁIU/ml) was blocked by a pre-incubation with TNFα (98.5% and 87.3%, respectively compared with TNFα alone), but still increased in the presence of GH (173.6% and 166.1%, respectively compared with GH alone). These studies suggest that GH and TNFα may have differential local effects on IGF/insulin-mediated actions in peripheral skeletal muscle. TNFα appears to be detrimental to IGF/insulin stimulated survival, differentiation and glucose metabolism, whereas GH appears to be facilitative to mitogenic/metabolic IGF/insulin mediated events.

  2. #2
    jbigdog69's Avatar
    jbigdog69 is offline Banned
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    Good read Bro...Thanks

  3. #3
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    This is an excellent post for a number of reasons. It's well-known that GH increases TNF-alpha, and it's well-known that TNF-alpha is a condributor or at least an indicator of something which directly causes insulin resistance (most likely TNF-alpha itself though). Increased levels of adiponectin mreduce insulin resistance. Adiponectin and TNF-alpha have an inverse relationship. Things like Avandia increase adiponectin and decrease TNF-alpha levels.

    What people also fail to consider is duration and localization. GH itself has a very short half-life, although the subsequent spike in IGF-1 levels persist for much longer. GH itself is what is implicated in causing insulin resistance, although acute, meaning a quick increase in insulin resistance with each administration. Long-term use of GH has also been said to cause insulin resistance, but this is independent of the acute effects of GH.

    So, we inject into adipose (abdominal). Although this study didn't show increased acute insulin resistance, it only was testing in myoblasts and not adipocytes (where this was originally discovered to be true). By injecting post workout into adipose, we could very well be inducing an acute period of insulin resistance in the vicinity of injection.....when using insulin concurrently, which is highly capable of storing excess carbs in adipocytes as well as myocytes, the increased TNF-alpha induced by the GH in the abdominal adipocytes may help prevent the uptake of carbs (glucose) into the abdominal adipocytes, thus helping to acheive leaner gains with insulin. Granted, we have no quantification of the duration of increased TNF-alpha (and this study, like I said, is with myoblasts not adipocytes, so doesn't show increased TNF-alpha at all) or the measure of how far-reaching these localized effects may be....maybe just a few square cm, but the point is.....it's yet another reason to use GH with insulin, although somewhat minor in contrast to the other reasons.

  4. #4
    Toemonster is offline New Member
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    Do you think using GH for 6 months or more by itself will cause any problems with your insulin ?

  5. #5
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    Quote Originally Posted by Toemonster
    Do you think using GH for 6 months or more by itself will cause any problems with your insulin?
    Nope. I know both Mallet and myself have used GH for long periods and measure BG values, and neither of us have seen any variations in BG values over time to indicate such a thing. Possibly higher doses over a 6 month period could, but that's just speculation.

  6. #6
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    Thumbs up

    "So, we inject into adipose (abdominal). "

    so are you saying that you inject subq with GH? Why not inj IM?

  7. #7
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    Quote Originally Posted by Tank010101
    "So, we inject into adipose (abdominal). "

    so are you saying that you inject subq with GH? Why not inj IM?
    For the localized lipolytic effects....some don't see the spot reduction of fat, but some see very pronounced effects. You can certainly go IM though.

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