Impact of Growth Hormone Administration on Other Hormonal Axes

Jørgensen, Jens Otto Lunde; Ovesen, Per; Juul, Anders; Hansen, Troels Krarup; Skakkebæk, Niels E.; Js, Christiansen

doi:10.1159/000053174

Cited by 14 publications

(15 citation statements)

References 25 publications

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“…Another indirect effect of GH is the enhancement of the conversion of T 4 to tri-iodothyronine (T 3 ) via upregulation of deiodinase enzyme (27). The combined treatment of GH and ½T4 þ GC used in the present study may therefore result in increased plasma levels of T 3 (28).…”

Section: Enos Expression and Localisationmentioning

confidence: 88%

GH and IGF-I regulate the expression of endothelial nitric oxide synthase (eNOS) in cardiovascular tissues of hypophysectomized female rats

Wickman

Jonsdottir

Bergström

et al. 2002

European Journal of Endocrinology

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Objective: This study explored whether short-term replacement therapy with growth hormone (GH) affects blood pressure (BP), heart rate (HR) and endothelial nitric oxide synthase (eNOS) expression in cardiovascular tissues in hypophysectomized (Hx) female rats. Design and Methods: BP, HR and the expression of eNOS in the aorta, caval vein and heart were studied in Hx female rats and in Hx female rats that underwent 7 days treatment with GH and thyroxine þ glucocorticoids ð½T 4 þ GCÞ: Insulin-like growth factor-I (IGF-I) was included in a second experimental protocol to explore the indirect effect of GH. The expression and localisation of eNOS was analysed by immunoblotting and immunohistochemistry. Results: Decreased BP (Hx 98^1; Intact 129^3 mmHg; P , 0:05), HR (Hx 297^14; Intact 399^31 beats=min; P , 0:05) and unchanged eNOS expression was demonstrated in Hx compared with intact rats. None of the hormones affected BP, but both GH and IGF-I increased HR compared with Hx rats (GH 358^10; IGF-I 337^7; Hx 306^11 beats=min; P , 0:05). Replacement of GH, GH þ ½T 4 þ GC and IGF-I resulted in an increased aortic eNOS expression (GH 161^24; GH þ ½T 4 þ GC 177^25; IGF-I 153^21; Hx 109^7%; P , 0:05), whereas in caval vein only GH þ ½T 4 þ GC affected eNOS expression. None of the hormones changed the level of eNOS in the heart. eNOS was localised in the intima layer of the aorta, whereas in the caval vein eNOS was localised in all cell layers. Conclusions: These findings support the suggested positive role of GH in the regulation of the cardiovascular homeostasis. The observed up-regulation of eNOS, and presumably an increased NO bioavailability, may result in improved endothelial and cardiovascular function.

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Section: Enos Expression and Localisationmentioning

confidence: 88%

GH and IGF-I regulate the expression of endothelial nitric oxide synthase (eNOS) in cardiovascular tissues of hypophysectomized female rats

Wickman

Jonsdottir

Bergström

et al. 2002

European Journal of Endocrinology

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“…GH has a regulatory effect on several other hormonal systems, while changes in other pituitary or peripheral hormones could influence GH and IGF-I levels [25]. GH is a physiological regulator of thyroid hormone metabolism and has a direct or indirect (through IGF-I) stimulatory effect on T 4 to T 3 conversion.…”

Section: Discussionmentioning

confidence: 99%

Effect of Growth Hormone Replacement Therapy on Pituitary Hormone Secretion and Hormone Replacement Therapies in GHD Adults

Hubina¹,

Mersebach

Rasmussen

et al. 2004

Horm Res Paediatr

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Objective: We tested the impact of commencement of GH replacement therapy in GH-deficient (GHD) adults on the circulating levels of other anterior pituitary and peripheral hormones and the need for re-evaluation of other hormone replacement therapies, especially the need for dose changes. Methods: 22 GHD patients were investigated in a double-blind randomized study and 90 GHD patients in an open study at baseline and after 6 and 12 months of GH replacement therapy. Results: In the placebo-controlled trial, the FT₃ levels increased after 6 months in the GH-treated group, and in the open study the FT₃ levels tended to increase. Other hormone concentrations did not change in either part of the study. Four patients required an increase in thyroxine dose, while 2 patients needed dose reduction. One originally euthyroid patient required thyroxine replacement. Two patients with originally conserved pituitary-adrenal function developed ACTH insufficiency. The hydrocortisone dose was increased in 1 and decreased in 1 of the 66 patients with secondary hypocortisolism. None of the females required any adjustment of sex hormone replacement therapy. Two of 37 males needed dose increase of testosterone, while 1 needed dose reduction. Conclusion: GH replacement therapy required dose adjustments regarding other hormone replacement therapies in 12.2% (n = 11), while initiation of new hormone replacement was performed in 3.3% (n = 3) of the 90 patients during the 1-year follow-up. Monitoring of pituitary hormone axes is advisable after commencement of GH replacement therapy, since changes of hormone replacement therapy was observed in a small but clinically significant number of patients.

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“…The etiology of the hypothyroidism was chronic autoimmune Hashimoto's thyroiditis (n = 37) and chronic atrophic thyroiditis (n = 3), postoperative hypothyroidism (n = 8), and painless thyroiditis (n = 3). The etiology of the hyperthyroidism was Graves disease (n = 10), toxic adenoma (n = 3), toxic multinodular goiter (n = 7), painless thyroiditis [5], and drug overdose [5]. A group of 37 euthyroid healthy subjects (mean age 40.6 ± 2.1 years) were studied as controls.…”

Section: Methodsmentioning

confidence: 99%

“…GH, in turn, mediates its effects by regulating the synthesis and secretion of IGF-I [2]. GH/IGF axis affects growth and function of the thyroid, as well as thyroid hormone metabolism [3][4][5]. GH also seems to play an important role, either directly or indirectly, in the regulation of peripheral T4 metabolism by GH-induced enhancement of peripheral deiodination of T4 to T3 [6].…”

Section: Introductionmentioning

confidence: 99%

Growth hormone/insulin-like growth factor axis in patients with subclinical thyroid dysfunction

Akın

Yaylalı

Turgut

et al. 2009

Growth Hormone & IGF Research

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Impact of Growth Hormone Administration on Other Hormonal Axes

Cited by 14 publications

References 25 publications

GH and IGF-I regulate the expression of endothelial nitric oxide synthase (eNOS) in cardiovascular tissues of hypophysectomized female rats

GH and IGF-I regulate the expression of endothelial nitric oxide synthase (eNOS) in cardiovascular tissues of hypophysectomized female rats

Effect of Growth Hormone Replacement Therapy on Pituitary Hormone Secretion and Hormone Replacement Therapies in GHD Adults

Growth hormone/insulin-like growth factor axis in patients with subclinical thyroid dysfunction

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