I don't think that resverartrol influences directly on the growth hormone (GH) itself. They (resverartrol and GH) are different signalling molecules with antagonistic action

There animal studies, some showing a increase in growth hormone or the related IGF-1, others show a decrease, so its hard to know what it will do in people, it might be biphasic, dose dependent. Here the abstracts I found:

Am J Vet Res. 2014 Aug;75(8):752-9. doi: 10.2460/ajvr.75.8.752.

Modulation of growth and immunity by dietary supplementation with resveratrol in young chickens receiving conventional vaccinations.

Zhang C1, Tian Y, Yan F, Kang X, Han R, Sun G, Zhang H.

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Abstract

OBJECTIVE:

To determine the effects of resveratrol (RES) on growth and immune status in chickens receiving conventional vaccinations.

ANIMALS:

Two hundred forty 1-day-old layer chickens.

PROCEDURES:

Chickens received conventional vaccinations throughout the study and were randomly assigned to 1 of 4 treatments in 6 replicate pens/treatment. Treatments included 1 control group (basal diet) and 3 experimental groups fed the basal diet plus 200, 400, and 800 mg of RES/kg of diet. At 40 days of age, 1 bird/pen was randomly selected to have blood and tissues collected to determine serum immunity indices; mRNA relative expression of proinflammatory cytokines in splenocytes; mRNA relative expression of nuclear transcription factor-κB, growth hormone receptor, and insulin-like growth factor-1 in hepatocytes; cell proliferation; and apoptosis.

RESULTS:

Average daily gain, antibody titers against Newcastle disease virus and avian influenza viruses H5 and H9, and insulin-like growth factor-1 expression were quadratically increased with increasing RES concentration. In hepatocytes, growth hormone receptor gene mRNA relative expression was quadratically increased and nuclear transcription factor-κB gene mRNA relative expression was linearly decreased with increasing RES concentration. In splenocytes, nterleukin-1β and tumor necrosis factor-α mRNA relative expression was linearly decreased with increasing RES concentration. Resveratrol supplementation delayed cell proliferation and reduced apoptosis in immunocytes. With increasing RES concentration, proliferation index and relative weight of the thymus, ratio of CD4+ to CD8+ cells, and CD4+ cell count were quadratically increased, and IgM concentration was linearly increased.

CONCLUSIONS AND CLINICAL RELEVANCE:

Dietary resveratrol supplementation improved growth, protected immunocytes against antigen-induced apoptosis, and upregulated immune response in chickens that received conventional vaccinations.

PMID:

25061707

DOI:

10.2460/ajvr.75.8.752

[Indexed for MEDLINE]

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Select item 24570423 2.

Poult Sci. 2014 Jan;93(1):54-62. doi: 10.3382/ps.2013-03423.

Resveratrol induces antioxidant and heat shock protein mRNA expression in response to heat stress in black-boned chickens.

Liu LL1, He JH, Xie HB, Yang YS, Li JC, Zou Y.

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Abstract

This study investigated the effects of dietary resveratrol at 0, 200, 400, or 600 mg/kg of diet on the performance, immune organ growth index, serum parameters, and expression levels of heat shock protein (Hsp) 27, Hsp70, and Hsp90 mRNA in the bursa of Fabricius, thymus, and spleen of 42-d-old female black-boned chickens exposed to heat stress at 37 ± 2°C for 15 d. The results showed that heat stress reduced daily feed intake and BW gain; decreased serum glutathione (GSH), growth hormone, and insulin-like growth factor-1 levels; and inhibited GSH peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) activities compared with birds subjected to thermo-neutral circumstances. Chickens that were fed diets supplemented with resveratrol exhibited a linear increase in feed intake and BW gain (P < 0.001); serum GSH, growth hormone, and insulin-like growth factor-1 levels (P ≤ 0.01); and GSH-Px, SOD, and CAT activities (P < 0.001) compared with chickens that were fed diets without resveratrol during heat stress. In contrast, serum malonaldehyde concentrations were decreased (P < 0.001) in the chickens fed a resveratrol-supplemented diet. Heat stress also reduced (P < 0.05) the growth index of the bursa of Fabricus and spleen; however, it had no effect on the growth index of the thymus. The growth index of the bursa of Fabricius and spleen increased (P < 0.05) upon heat stress and coincided with an increase in supplemental resveratrol levels. The expression of Hsp27, Hsp70, and Hsp90 mRNA in the bursa of Fabricius and spleen were increased (P < 0.01), but those of Hsp27 and Hsp90 mRNA in thymus were decreased (P < 0.01) under heat stress compared with no heat stress. Resveratrol attenuated the heat stress-induced overexpression of Hsp27, Hsp70, and Hsp90 mRNA in the bursa of Fabricius and spleen and increased the low expression of Hsp27 and Hsp90 mRNA in thymus upon heat stress. The results suggest that supplemental resveratrol improves growth performance and reduces oxidative stress in heat-stressed black-boned chickens by increasing serum growth hormone concentrations and modulating the expression of heat shock genes in organs of the immune system.

KEYWORDS:

antioxidant response; black-boned chicken; heat shock protein; heat stress; resveratrol

PMID:

24570423

DOI:

10.3382/ps.2013-03423

[Indexed for MEDLINE]

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FASEB J. 2013 Apr;27(4):1561-71. doi: 10.1096/fj.12-220129. Epub 2013 Jan 4.

Sirt1 inhibits the transcription factor CREB to regulate pituitary growth hormone synthesis.

Monteserin-Garcia J1, Al-Massadi O, Seoane LM, Alvarez CV, Shan B, Stalla J, Paez-Pereda M, Casanueva FF, Stalla GK, Theodoropoulou M.

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Abstract

Growth hormone (GH) is a major anabolic hormone and the primary regulator of organism growth. Its transcription is triggered by GH-releasing hormone (GHRH) through the transcription factor cAMP response element-binding protein (CREB) and by caloric intake. In contrast, the deacetylase Sirt1 is activated by caloric restriction. Therefore, the present study investigates how Sirt1 affects CREB function and GH synthesis. Sirt1 pharmacological activation with resveratrol (IC₅₀=87 μM) suppressed GHRH-induced GH secretion from rat anterior pituitary cells in vivo and in vitro, while vehicle controls showed no effect. Resveratrol's effects were abolished after knocking down Sirt1 with RNA interference, but not in control scrambled siRNA-transfected rat somatotrophs, confirming the Sirt1 specificity. Sirt1 activation and overexpression suppressed forskolin-induced CREB-Ser(133) phosphorylation, but no effect was seen with vehicle and empty plasmid controls. The deacetylase-dead mutant Sirt1 retained CREB-Ser(133) phosphorylation by keeping protein phosphatase protein phosphatase 1 activity low. Sirt1 activation suppressed glycogen synthase kinase 3 β acetylation, and a mutation on the GSK3β-Lys(205) residue mimicking a hypoacetylated form revealed increased activity. In summary, this is a novel mechanism through which Sirt1 intercepts the cAMP pathway by suppressing CREB transcriptional activation, resulting in decreased GH synthesis.

PMID:

23292070

DOI:

10.1096/fj.12-220129

[Indexed for MEDLINE]

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Carcinogenesis. 2007 Sep;28(9):1946-53. Epub 2007 Aug 3.

Resveratrol suppresses prostate cancer progression in transgenic mice.

Harper CE1, Patel BB, Wang J, Arabshahi A, Eltoum IA, Lamartiniere CA.

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Abstract

Resveratrol, a natural polyphenolic phytochemical, has been reported to act as an antioxidant and provide anticancer activities. We hypothesized that resveratrol would exert a chemopreventive effect against prostate cancer via regulation of sex steroid receptor and growth factor signaling pathways. In the current study, Transgenic Adenocarcinoma Mouse Prostate males were fed resveratrol (625 mg resveratrol per kg AIN-76A diet) or phytoestrogen-free, control diet (AIN-76A) starting at 5 weeks of age. Mechanisms of action and histopathology studies were conducted at 12 and 28 weeks of age, respectively. Resveratrol in the diet significantly reduced the incidence of poorly differentiated prostatic adenocarcinoma by 7.7-fold. In the dorsolateral prostate, resveratrol significantly inhibited cell proliferation, increased androgen receptor, estrogen receptor-beta, and insulin-like growth factor-1 receptor, and significantly decreased insulin-like growth factor (IGF)-1 and phospho-extracellular regulating kinase 1 (phospho-ERK 1). In the ventral prostate, resveratrol significantly reduced cell proliferation and phospho-ERKs 1 and 2, but did not significantly alter insulin-like growth factor-1 receptor and IGF-1. Serum total testosterone, free testosterone, estradiol, dihydrotestosterone and sex hormone-binding globulin (SHBG) concentrations and Simian Virus-40 large T antigen expression in the prostate were not altered in resveratrol-treated mice. Total resveratrol concentration in the blood serum of 12-week-old mice treated for 3 weeks with 625 mg resveratrol per kg diet was 52 +/- 18 nM. The decrease in cell proliferation and the potent growth factor, IGF-1, the down-regulation of downstream effectors, phospho-ERKs 1 and 2 and the increase in the putative tumor suppressor, estrogen receptor-beta, provide a biochemical basis for resveratrol suppressing prostate cancer development.

PMID:

17675339

DOI:

10.1093/carcin/bgm144

[Indexed for MEDLINE]

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Nutr Metab (Lond). 2010 May 10;7:40. doi: 10.1186/1743-7075-7-40.

Subchronic exposure to phytoestrogens alone and in combination with diethylstilbestrol - pituitary tumor induction in Fischer 344 rats.

Jeng YJ1, Kochukov M, Nauduri D, Kaphalia BS, Watson CS.

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Abstract

BACKGROUND:

Subchronic administration of the potent pharmaceutical estrogen diethylstilbestrol (DES) to female Fischer 344 (F344) rats induces growth of large, hemorrhagic pituitaries that progress to tumors. Phytoestrogens (dietary plant estrogens) are hypothesized to be potential tumor inhibitors in tissues prone to estrogen-induced cancers, and have been suggested as "safer" estrogen replacements. However, it is unknown if they might themselves establish or exacerbate the growth of estrogen-responsive cancers, such as in pituitary.

METHODS:

We implanted rats with silastic capsules containing 5 mg of four different phytoestrogens - either coumestrol, daidzein, genistein, or trans-resveratrol, in the presence or absence of DES. We examined pituitary and other organ weights, blood levels of prolactin (PRL) and growth hormone (GH), body weights, and pituitary tissue histology.

RESULTS:

Blood level measurements of the administered phytoestrogens confirmed successful exposure of the animals to high levels of these compounds. By themselves, no phytoestrogen increased pituitary weights or serum PRL levels after 10 weeks of treatment. DES, genistein, and resveratrol increased GH levels during this time. Phytoestrogens neither changed any wet organ weight (uterus, ovary, cervix, liver, and kidney) after 10 weeks of treatment, nor reversed the adverse effects of DES on pituitaries, GH and PRL levels, or body weight gain after 8 weeks of co-treatment. However, they did reverse the DES-induced weight increase on the ovary and cervix. Morphometric examination of pituitaries revealed that treatment with DES, either alone or in combination with phytoestrogens, caused gross structural changes that included decreases in tissue cell density, increases in vascularity, and multiple hemorrhagic areas. DES, especially in combination with phytoestrogens, caused the development of larger and more heterogeneous nuclear sizes in pituitary.

CONCLUSIONS:

High levels of phytoestrogens by themselves did not cause pituitary precancerous growth or change weights of other estrogen-sensitive organs, though when combined with DES, they counteracted the growth effects of DES on reproductive organs. In the pituitary, phytoestrogens did not reverse the effects of DES, but they did increase the sizes and size heterogeneity of nuclei. Therefore, phytoestrogens may oppose some but not all estrogen-responsive tissue abnormalities caused by DES overstimulation, and appear to exacerbate DES-induced nuclear changes.

PMID:

20459739

PMCID:

PMC2881934

DOI:

10.1186/1743-7075-7-40

Free PMC Article

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