Human Plasma Growth Hormone (GH)-Binding Proteins Are Regulated by GH and Testosterone*

Postel-Vinay, Marie-Catherine; Tar, Attila; Hocquette, Jean‐François; Clot, Jean-Pierre; Fontoura, Manuel; Brauner, Raja; Rappaport, R

doi:10.1210/jcem-73-1-197

Cited by 83 publications

(52 citation statements)

References 20 publications

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“…Some reports showed that there was a negative correlation between GHBP levels and GH secretion, which suggested that a decrease in GH secretion could increase GH sensitivity and the up-regulation of the GH receptor compensating for impairment of GH secretion (24,25). In our study, IGF-I levels did not decrease in obese subjects, despite GH hyposecretion, and they showed a significant positive correlation with GHBP.…”

Section: Lean Ngtsupporting

confidence: 47%

GH-binding protein in obese men with varying glucose tolerance: relationship to body fat distribution, insulin secretion and the GH-IGF-I axis

Nam

Kim

Song

et al. 1999

European Journal of Endocrinology

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Bioelectrical impedance for measurement of total body fat and computed tomography for visceral and subcutaneous fat at umbilicus levels were performed in 34 obese and 10 lean men. Insulin secretion in response to an oral glucose tolerance test (OGTT) and a GH stimulation test by L-dopa, growth hormone-binding protein (GHBP) and IGF-I were measured. Obese subjects were divided into three groups according to the OGTT. The obese type II diabetes mellitus group had the highest GHBP levels and the most visceral fat. GHBP levels were most strongly correlated with the ratio of visceral fat area to body weight (VWR) above any other parameters (r = 0.725, P < 0.001). The insulin and free fatty acid (FFA) areas under curves (AUC) during the OGTT, and the IGF-I level, were also positively correlated with GHBP levels (r = 0.474, P < 0.005; r = 0.572, P < 0.005; r = 0.453, P < 0.005). GH-AUC to the L-dopa stimulation test was negatively correlated with GHBP levels (r = ¹0.432, P < 0.005). Stepwise multiple linear regression analysis showed that VWR, FFA-AUC and insulin-AUC significantly contributed to the variability of GHBP (r 2 = 0.58). In conclusion, we demonstrated that: (i) visceral fat amount mainly determined GHBP levels in obese men with varying glucose tolerance; (ii) hyperglycemia per se did not influence the GHBP level, whereas insulin and FFA could play a role in regulation of GHBP; and (iii) although GH was not the main regulator of GHBP, the unchanged IGF-I level despite GH hyposecretion suggests that increased GHBP levels reflect GH hypersensitivity in order to compensate for decreased GH secretion in obesity.

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Section: Lean Ngtsupporting

confidence: 47%

GH-binding protein in obese men with varying glucose tolerance: relationship to body fat distribution, insulin secretion and the GH-IGF-I axis

Nam

Kim

Song

et al. 1999

European Journal of Endocrinology

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“…GH receptor levels are sensitive to gonadal steroids, but data from previous studies on the nature of this effect are contradictory. Testosterone administration induced an elevation in hepatic GH receptor mRNA levels in rabbits (Yu et al 1996), a decrease in GH-binding protein (GHBP) in man (Postel-Vinay et al 1991) and no change in hepatic GH receptor mRNA or circulating GHBP in rats (Carmignac et al 1993).…”

Section: Introductionmentioning

confidence: 99%

Testosterone effect on growth and growth mediators of the GH-IGF-I axis in the liver and epiphyseal growth plate of juvenile rats

Zung

Phillip²,

Chalew³

et al. 1999

Journal of Molecular Endocrinology

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Several studies have suggested that testosterone may have a direct, GH-independent effect on growth. In order to assess possible mechanism(s) whereby testosterone exerts its growth-promoting effect, we evaluated its effect on growth mediators of the GH-IGF-I axis, in both the liver and the epiphyseal growth plate (EGP). Testosterone was administered to peripubertal rats and the responses of mRNA of GH receptor, IGF-I, IGF-I receptor and IGF-binding proteins-1 and -3 (IGFBP-1 and IGFBP-3) as well as circulating IGF-I were evaluated in two time-related models: over 12 h after a single injection (short-term study) and 10 days after continuous administration (long-term study). Rats in the short-term study were castrated and were killed 1, 4, 6 and 12 h post injection. Rats in the long-term study were divided into two groups: castrated vs castrated and hypophysectomized, in order to assess the effect of testosterone in the presence and absence of GH. mRNA levels were determined by RNase protection assay, and serum IGF-I by RIA.Testosterone enhanced weight gain in the rats treated for 10 days, a change that was similar in the presence or absence of GH. This effect was relatively small, however, by comparison with the total weight gained without testosterone. Testosterone had no effect on hepatic IGF-I mRNA abundance but induced a reduction in circulating IGF-I levels, in both the short-and long-term study. Testosterone had no effect on hepatic GH receptor and IGFBP-3 mRNA levels but resulted in a transient, short-term elevation in IGFBP-1 mRNA levels that was maximal 4 h post injection.In the EGP, neither testosterone administration nor hypophysectomy had any effect on IGF-I and IGF-I receptor mRNA levels. However, testosterone increased GH receptor mRNA abundance after 10 days of continuous administration in hypophysectomized rats only.These data suggest that the effect of testosterone on growth (as assessed by weight gain) is small and is not mediated by changes in hepatic gene expression of IGF-I, IGF-I receptor, IGFBP-1, IGFBP-3 or circulating IGF-I. At the EGP, the testosterone effect on linear growth is not mediated through changes in mRNA abundance of IGF-I and IGF-I receptor. The small but significant elevation of GH receptor mRNA levels in hypophysectomized rats may suggest a testosterone-mediated augmentation of a GH effect at the target organ.

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“…In addition, it has been shown that the levels of this protein are up-regulated by GH (18,19). Few and conflicting data are available on the plasma GH-BP activity in girls with Turner's syndrome.…”

mentioning

confidence: 99%

Plasma Growth Hormone-Binding Protein Activity, Insulin-like Growth Factor I, and Its Binding Protein Levels in Patients with Turner's Syndrome: Effect of Short- and Long-Term Recombinant Human Growth Hormone Administration

1995

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Plasma growth hormone-binding protein (GH-BP) activity and the levels of IGF-I and its binding proteins (IGFBP) were studied in eight girls with Turner's syndrome before and during recombinanthGH (r-hGH) administration. Growth hormone and GH-BP activity were assayed at baseline and hourly, over a 12-h period, after an intramuscular bolus of 0.09 mgikg of the hormone. After 7 d, each patient received r-hGH at 0.33 mgikg/weekly s.c. every day at nighttime; plasma growth hormone-binding protein activity, blood IGF-I, and IGFBP were evaluated before and on d 7, 30, 180, and 360. Baseline reference values were obtained from 10 bone agematched healthy girls. Basal GH-BP activity, IGF-I, and IGFBP levels were similar in patients and controls. Four h after the intramuscular injection, GH-BP activity maximally increased and returned to baseline 6-7 h later; during long-term r-hGH administration GH-BP activity peaked at + 180 d but declined to pretreatment at +360 d. IGF-I, IGFBP-3, and IGFBP-4 increased under r-hGH and, in contrast to GH-BP activity, remained high throughout the study. In conclusion, in girls with Turner's syndrome, GH-BP activity, IGF-I, IGFBP-3, and IGFBP-4 are induced by r-hGH. However, the increase of IGF-I and IGFBP-3 does not require an increased level of the cellular growth hormone receptors, as suggested by the unchanged +360 d values of plasma GH-BP activity compared with baseline. The absence of an association among any of the biochemical parameters studied and the growth of the patients taking r-hGH suggests that a peripheral defect may affect their growth. (Pediatr Res 37: 106111, 1995)

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Human Plasma Growth Hormone (GH)-Binding Proteins Are Regulated by GH and Testosterone*

Cited by 83 publications

References 20 publications

GH-binding protein in obese men with varying glucose tolerance: relationship to body fat distribution, insulin secretion and the GH-IGF-I axis

GH-binding protein in obese men with varying glucose tolerance: relationship to body fat distribution, insulin secretion and the GH-IGF-I axis

Testosterone effect on growth and growth mediators of the GH-IGF-I axis in the liver and epiphyseal growth plate of juvenile rats

Plasma Growth Hormone-Binding Protein Activity, Insulin-like Growth Factor I, and Its Binding Protein Levels in Patients with Turner's Syndrome: Effect of Short- and Long-Term Recombinant Human Growth Hormone Administration

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