Neuroendocrine alterations in the somatotropic and lactotropic axes in uremic men

Johannes D Veldhuis, A. Iranmanesh, M. J. Wilkowski, E. Samojlik

Research output: Contribution to journalArticle

59 Citations (Scopus)

Abstract

To investigate the pathophysiology of altered growth hormone (GH) and prolactin secretion in end-stage renal disease, we sampled blood at 10-min intervals for 24 h and applied deconvolution analysis to calculate hormone half-lives and pulsatile secretion rates. Two-site immunoradiometric assays were employed to quantitate presumptively intact GH and prolactin in nine middle-aged men with chronic renal failure and 14 gender-, age-, body weight- and community-matched controls. We observed that the half-lives of endogenous GH and prolactin were prolonged significantly in uremia: for GH, control 17 ± 1.4 versus uremia 21 ± 1.3 min (p < 0.05); for prolactin, control 66 ± 9.3 versus uremia 112 ± 10 min (p < 0.01). Daily GH secretion rates exceeded sex-, age- and weight-predicted values in eight of nine uremic individuals, while values for prolactin were variable but on average twofold higher in uremia. In both the somatotropic and lactotropic axes, the frequency of secretory bursts was increased significantly (for GH, control 11 ± 1.1 versus uremia 15 ± 0.84 secretory events/24 h: for prolactin, control 20 ± 0.90 versus uremia 27 ± 1.3 pulses/24 h, p < 0.05). Although there were no significant alterations in the mean amplitude, duration or mass of GH secretory bursts, prolactin secretory burst amplitudes were elevated threefold in uremia (p < 0.01). These distinctive mechanisms brought about higher 24-h mean serum concentrations of GH (0.70 ± 0.17 control versus 1.22 ± 0.32 μg/l uremia) and prolactin (7.3 ± 2.4 control versus 26 ± 6.1 μg/l uremia, p < 0.05). Lastly, serum concentrations of estradiol were increased but those of unconjugated estriol decreased in uremia. We conclude that hypersomatotropinemia and hyperprolactinemia in uremic men result from prolonged hormone half-lives combined with increased frequencies of secretory events driven by unknown stimuli within the respective axes, and/or by defects in their negative-feedback regulation. We postulate that the latter may arise from partial tissue resistance to hormone action in hemodialyzed men.

Original languageEnglish (US)
Pages (from-to)489-498
Number of pages10
JournalEuropean Journal of Endocrinology
Volume131
Issue number5
StatePublished - 1994
Externally publishedYes

Fingerprint

Uremia
Prolactin
Growth Hormone
Hormones
Chronic Kidney Failure
Immunoradiometric Assay
Estriol
Hyperprolactinemia
Serum
Estradiol
Body Weight
Weights and Measures

ASJC Scopus subject areas

  • Endocrinology

Cite this

Veldhuis, J. D., Iranmanesh, A., Wilkowski, M. J., & Samojlik, E. (1994). Neuroendocrine alterations in the somatotropic and lactotropic axes in uremic men. European Journal of Endocrinology, 131(5), 489-498.

Neuroendocrine alterations in the somatotropic and lactotropic axes in uremic men. / Veldhuis, Johannes D; Iranmanesh, A.; Wilkowski, M. J.; Samojlik, E.

In: European Journal of Endocrinology, Vol. 131, No. 5, 1994, p. 489-498.

Research output: Contribution to journalArticle

Veldhuis, JD, Iranmanesh, A, Wilkowski, MJ & Samojlik, E 1994, 'Neuroendocrine alterations in the somatotropic and lactotropic axes in uremic men', European Journal of Endocrinology, vol. 131, no. 5, pp. 489-498.
Veldhuis JD, Iranmanesh A, Wilkowski MJ, Samojlik E. Neuroendocrine alterations in the somatotropic and lactotropic axes in uremic men. European Journal of Endocrinology. 1994;131(5):489-498.
Veldhuis, Johannes D ; Iranmanesh, A. ; Wilkowski, M. J. ; Samojlik, E. / Neuroendocrine alterations in the somatotropic and lactotropic axes in uremic men. In: European Journal of Endocrinology. 1994 ; Vol. 131, No. 5. pp. 489-498.
@article{8a95a3480f91436d96495ce5f2bcc80c,
title = "Neuroendocrine alterations in the somatotropic and lactotropic axes in uremic men",
abstract = "To investigate the pathophysiology of altered growth hormone (GH) and prolactin secretion in end-stage renal disease, we sampled blood at 10-min intervals for 24 h and applied deconvolution analysis to calculate hormone half-lives and pulsatile secretion rates. Two-site immunoradiometric assays were employed to quantitate presumptively intact GH and prolactin in nine middle-aged men with chronic renal failure and 14 gender-, age-, body weight- and community-matched controls. We observed that the half-lives of endogenous GH and prolactin were prolonged significantly in uremia: for GH, control 17 ± 1.4 versus uremia 21 ± 1.3 min (p < 0.05); for prolactin, control 66 ± 9.3 versus uremia 112 ± 10 min (p < 0.01). Daily GH secretion rates exceeded sex-, age- and weight-predicted values in eight of nine uremic individuals, while values for prolactin were variable but on average twofold higher in uremia. In both the somatotropic and lactotropic axes, the frequency of secretory bursts was increased significantly (for GH, control 11 ± 1.1 versus uremia 15 ± 0.84 secretory events/24 h: for prolactin, control 20 ± 0.90 versus uremia 27 ± 1.3 pulses/24 h, p < 0.05). Although there were no significant alterations in the mean amplitude, duration or mass of GH secretory bursts, prolactin secretory burst amplitudes were elevated threefold in uremia (p < 0.01). These distinctive mechanisms brought about higher 24-h mean serum concentrations of GH (0.70 ± 0.17 control versus 1.22 ± 0.32 μg/l uremia) and prolactin (7.3 ± 2.4 control versus 26 ± 6.1 μg/l uremia, p < 0.05). Lastly, serum concentrations of estradiol were increased but those of unconjugated estriol decreased in uremia. We conclude that hypersomatotropinemia and hyperprolactinemia in uremic men result from prolonged hormone half-lives combined with increased frequencies of secretory events driven by unknown stimuli within the respective axes, and/or by defects in their negative-feedback regulation. We postulate that the latter may arise from partial tissue resistance to hormone action in hemodialyzed men.",
author = "Veldhuis, {Johannes D} and A. Iranmanesh and Wilkowski, {M. J.} and E. Samojlik",
year = "1994",
language = "English (US)",
volume = "131",
pages = "489--498",
journal = "European Journal of Endocrinology",
issn = "0804-4643",
publisher = "BioScientifica Ltd.",
number = "5",

}

TY - JOUR

T1 - Neuroendocrine alterations in the somatotropic and lactotropic axes in uremic men

AU - Veldhuis, Johannes D

AU - Iranmanesh, A.

AU - Wilkowski, M. J.

AU - Samojlik, E.

PY - 1994

Y1 - 1994

N2 - To investigate the pathophysiology of altered growth hormone (GH) and prolactin secretion in end-stage renal disease, we sampled blood at 10-min intervals for 24 h and applied deconvolution analysis to calculate hormone half-lives and pulsatile secretion rates. Two-site immunoradiometric assays were employed to quantitate presumptively intact GH and prolactin in nine middle-aged men with chronic renal failure and 14 gender-, age-, body weight- and community-matched controls. We observed that the half-lives of endogenous GH and prolactin were prolonged significantly in uremia: for GH, control 17 ± 1.4 versus uremia 21 ± 1.3 min (p < 0.05); for prolactin, control 66 ± 9.3 versus uremia 112 ± 10 min (p < 0.01). Daily GH secretion rates exceeded sex-, age- and weight-predicted values in eight of nine uremic individuals, while values for prolactin were variable but on average twofold higher in uremia. In both the somatotropic and lactotropic axes, the frequency of secretory bursts was increased significantly (for GH, control 11 ± 1.1 versus uremia 15 ± 0.84 secretory events/24 h: for prolactin, control 20 ± 0.90 versus uremia 27 ± 1.3 pulses/24 h, p < 0.05). Although there were no significant alterations in the mean amplitude, duration or mass of GH secretory bursts, prolactin secretory burst amplitudes were elevated threefold in uremia (p < 0.01). These distinctive mechanisms brought about higher 24-h mean serum concentrations of GH (0.70 ± 0.17 control versus 1.22 ± 0.32 μg/l uremia) and prolactin (7.3 ± 2.4 control versus 26 ± 6.1 μg/l uremia, p < 0.05). Lastly, serum concentrations of estradiol were increased but those of unconjugated estriol decreased in uremia. We conclude that hypersomatotropinemia and hyperprolactinemia in uremic men result from prolonged hormone half-lives combined with increased frequencies of secretory events driven by unknown stimuli within the respective axes, and/or by defects in their negative-feedback regulation. We postulate that the latter may arise from partial tissue resistance to hormone action in hemodialyzed men.

AB - To investigate the pathophysiology of altered growth hormone (GH) and prolactin secretion in end-stage renal disease, we sampled blood at 10-min intervals for 24 h and applied deconvolution analysis to calculate hormone half-lives and pulsatile secretion rates. Two-site immunoradiometric assays were employed to quantitate presumptively intact GH and prolactin in nine middle-aged men with chronic renal failure and 14 gender-, age-, body weight- and community-matched controls. We observed that the half-lives of endogenous GH and prolactin were prolonged significantly in uremia: for GH, control 17 ± 1.4 versus uremia 21 ± 1.3 min (p < 0.05); for prolactin, control 66 ± 9.3 versus uremia 112 ± 10 min (p < 0.01). Daily GH secretion rates exceeded sex-, age- and weight-predicted values in eight of nine uremic individuals, while values for prolactin were variable but on average twofold higher in uremia. In both the somatotropic and lactotropic axes, the frequency of secretory bursts was increased significantly (for GH, control 11 ± 1.1 versus uremia 15 ± 0.84 secretory events/24 h: for prolactin, control 20 ± 0.90 versus uremia 27 ± 1.3 pulses/24 h, p < 0.05). Although there were no significant alterations in the mean amplitude, duration or mass of GH secretory bursts, prolactin secretory burst amplitudes were elevated threefold in uremia (p < 0.01). These distinctive mechanisms brought about higher 24-h mean serum concentrations of GH (0.70 ± 0.17 control versus 1.22 ± 0.32 μg/l uremia) and prolactin (7.3 ± 2.4 control versus 26 ± 6.1 μg/l uremia, p < 0.05). Lastly, serum concentrations of estradiol were increased but those of unconjugated estriol decreased in uremia. We conclude that hypersomatotropinemia and hyperprolactinemia in uremic men result from prolonged hormone half-lives combined with increased frequencies of secretory events driven by unknown stimuli within the respective axes, and/or by defects in their negative-feedback regulation. We postulate that the latter may arise from partial tissue resistance to hormone action in hemodialyzed men.

UR - http://www.scopus.com/inward/record.url?scp=0028173274&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028173274&partnerID=8YFLogxK

M3 - Article

VL - 131

SP - 489

EP - 498

JO - European Journal of Endocrinology

JF - European Journal of Endocrinology

SN - 0804-4643

IS - 5

ER -