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Permissive Action of Growth Hormone on the Renal Response to Dietary Phosphorus Deprivation

Permissive Action of Growth Hormone on the Renal Response to Dietary Phosphorus Deprivation Animal studies have shown that GH is necessary for the increased renal production of calcitriol during dietary phosphorus deprivation (PD). These studies suggest that this adaptive change in vitamin D metabolism is mediated through insulin-like growth factor-I (IGF-I) and/or insulin. We subjected 16 GH-deficient children to 96 h of severe dietary PD twice, first before and again during recombinant GH replacement. Half of the children received low dose and half received high dose replacement with recombinant GH. We measured renal tubular reabsorption maximum for phosphate corrected for glomerular filtration rate (TmP/GFR), PTH, IGF-I, calcidiol, and calcitriol pre- and postdietary PD, both off and on GH. We also assessed insulin secretion during an oral glucose load (OGTT) off and on GH. Basal PTH, calcidiol, calcitriol, and fasting blood sugar were unaffected by GH therapy. PD did not affect PTH or calcidiol either off or on GH. Basal TmP/GFR rose on GH therapy (4.8 ± 0.2 to 6.3 ± 0.4 mg/dL) and with PD (4.8 ± 0.2 to 5.7 ± 0.2 mg/dL off and 6.3 ± 0.4 to 7.8 ± 0.3 mg/dL on GH). The increments due to PD and GH therapy were additive. The increments on GH were independent of the GH dose. Before GH replacement, calcitriol did not rise during PD (22.3 ± 2.1 to 23.3 ±1.9 pg/mL), but during GH therapy, PD caused a significant rise in calcitriol (23.8 ± 2.5 to 33.3 ± 2.4 pg/mL; P < 0.0001). The increment in calcitriol during PD was significantly greater in the high dose than it was in the low dose group (11.7 ± 1.5 vs. 7.2 ± 1.6 pg/mL; P < 0.05). GH therapy caused a rise in the IGF-I level that was significantly greater in the high dose (0.26 ± 0.03 to 3.15 ± 0.56 U/mL) than in the low dose (0.27 ± 0.02 to 0.68 ± 0.13 U/mL) group. Insulin in response to OGTT was significantly greater after GH therapy (4155 ± 600 μU/mL·min off GH; 6504 ± 1153 μU/mL·min on GH), although there was no difference between the low and high dose groups. Regression analysis demonstrated a correlation between the change in calcitriol during PD and the IGF-I level (r = 0.83). There was no correlation between insulin levels and the change in calcitriol or between IGF-I or insulin levels and the increment in TmP/GFR during GH therapy. We conclude that 1) GH exerts an effect on the kidney to cause phosphorus conservation, which may be a direct effect; 2) phosphorus conservation in response to PD is independent of GH in humans; 3) increased calcitriol generation in response to PD is dependent upon GH; 4) the increment in calcitriol during PD correlates significantly with IGF-I levels, but not with insulin, suggesting that it may be an IGF-I-mediated effect of GH. This content is only available as a PDF. Author notes * This work was supported by NIH Grant RR-6020 (to the Pediatric Clinical Research Center) and NCI Grant CA-29502 (to the Core Nutritional Research Unit). Copyright © 1990 by The Endocrine Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Clinical Endocrinology and Metabolism Oxford University Press

Permissive Action of Growth Hormone on the Renal Response to Dietary Phosphorus Deprivation

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References (21)

Publisher
Oxford University Press
Copyright
Copyright © 1990 by The Endocrine Society
ISSN
0021-972X
eISSN
1945-7197
DOI
10.1210/jcem-70-4-1035
Publisher site
See Article on Publisher Site

Abstract

Animal studies have shown that GH is necessary for the increased renal production of calcitriol during dietary phosphorus deprivation (PD). These studies suggest that this adaptive change in vitamin D metabolism is mediated through insulin-like growth factor-I (IGF-I) and/or insulin. We subjected 16 GH-deficient children to 96 h of severe dietary PD twice, first before and again during recombinant GH replacement. Half of the children received low dose and half received high dose replacement with recombinant GH. We measured renal tubular reabsorption maximum for phosphate corrected for glomerular filtration rate (TmP/GFR), PTH, IGF-I, calcidiol, and calcitriol pre- and postdietary PD, both off and on GH. We also assessed insulin secretion during an oral glucose load (OGTT) off and on GH. Basal PTH, calcidiol, calcitriol, and fasting blood sugar were unaffected by GH therapy. PD did not affect PTH or calcidiol either off or on GH. Basal TmP/GFR rose on GH therapy (4.8 ± 0.2 to 6.3 ± 0.4 mg/dL) and with PD (4.8 ± 0.2 to 5.7 ± 0.2 mg/dL off and 6.3 ± 0.4 to 7.8 ± 0.3 mg/dL on GH). The increments due to PD and GH therapy were additive. The increments on GH were independent of the GH dose. Before GH replacement, calcitriol did not rise during PD (22.3 ± 2.1 to 23.3 ±1.9 pg/mL), but during GH therapy, PD caused a significant rise in calcitriol (23.8 ± 2.5 to 33.3 ± 2.4 pg/mL; P < 0.0001). The increment in calcitriol during PD was significantly greater in the high dose than it was in the low dose group (11.7 ± 1.5 vs. 7.2 ± 1.6 pg/mL; P < 0.05). GH therapy caused a rise in the IGF-I level that was significantly greater in the high dose (0.26 ± 0.03 to 3.15 ± 0.56 U/mL) than in the low dose (0.27 ± 0.02 to 0.68 ± 0.13 U/mL) group. Insulin in response to OGTT was significantly greater after GH therapy (4155 ± 600 μU/mL·min off GH; 6504 ± 1153 μU/mL·min on GH), although there was no difference between the low and high dose groups. Regression analysis demonstrated a correlation between the change in calcitriol during PD and the IGF-I level (r = 0.83). There was no correlation between insulin levels and the change in calcitriol or between IGF-I or insulin levels and the increment in TmP/GFR during GH therapy. We conclude that 1) GH exerts an effect on the kidney to cause phosphorus conservation, which may be a direct effect; 2) phosphorus conservation in response to PD is independent of GH in humans; 3) increased calcitriol generation in response to PD is dependent upon GH; 4) the increment in calcitriol during PD correlates significantly with IGF-I levels, but not with insulin, suggesting that it may be an IGF-I-mediated effect of GH. This content is only available as a PDF. Author notes * This work was supported by NIH Grant RR-6020 (to the Pediatric Clinical Research Center) and NCI Grant CA-29502 (to the Core Nutritional Research Unit). Copyright © 1990 by The Endocrine Society

Journal

Journal of Clinical Endocrinology and Metabolism – Oxford University Press

Published: Apr 1, 1990

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