Nm. Wright et al., INCREASED SERUM 1,25-DIHYDROXYVITAMIN-D AFTER GROWTH-HORMONE ADMINISTRATION IS NOT PARATHYROID HORMONE-MEDIATED, Calcified tissue international, 61(2), 1997, pp. 101-103
To assess the effects of growth hormone (GH) on serum 1,25-dihydroxyvi
tamin D [1,25(OH)(2)D], we performed the following prospective crossov
er study in six healthy, young, adult, white men. During each of two a
dmissions for 21/2 days to a general clinical research center, subject
s were placed on a daily dietary calcium intake of 400 mg. Serum calci
um, phosphorus, 1,25(OH)(2)D, immunoreactive intact parathyroid hormon
e (PTH), insulin-like growth factor I(IGF-I), IGF binding protein 3 (I
GFBP3), tubular reabsorption of phosphate (TRP), and maximum tubular r
eabsorption of phosphate (TMP/GFR) were measured. Recombinant human GH
(rhGH, Humatrope) (25 mu g/kg/day subcutaneously for 1 week) was admi
nistered prior to and during one of the admissions. Results are expres
sed as mean +/- SEM. Whereas serum 1,25(OH)(2)D (58.9 +/- 7.7 versus 5
1.6 +/- 7.4 pg/ml, P < 0.01), serum phosphorus (4.5 +/- 0.1 versus 3.7
+/- 0.1 mg/dl, P < 0.01), TRP (92.0 +/- 0.5 versus 87.8 +/- 0.7 mg/dl
, P < 0.005), TMP/GFR (4.6 +/- 0.1 versus 3.5 +/- 0.2, P < 0.005), and
urinary calcium (602 +/- 49 versus 346 +/- 25 mg/day, P < 0.001) incr
eased significantly serum PTH decreased significantly (19.9 +/- 1.9 ve
rsus 26.8 +/- 4.0 pg/ml, P < 0.05) and serum calcium did not change wh
en subjects received rhGH. These findings indicate that in humans, GH
affects serum 1,25(OH)(2)D independently of circulating PTH and that t
his effect is mediated by IGF-I. We propose, therefore, that one poten
tial mechanism by which GH stimulates increases in bone mass is via mo
dest increases in serum 1,25(OH)(2)D.