Vitamin D increases circulating IGF1 in adults: potential implication for treatment of growth hormone deficiency.
Eur J Endocrinol. 2013 Sep 4.
Pietro Ameri pietroameri at unige.it, Andrea Giusti, Mara Boschetti, Marta Bovio, Claudia Teti, Giovanna Leoncini, Diego Ferone, Giovanni Murialdo and Francesco M Minuto
P Ameri, Department of Internal Medicine, University of Genova, Genova, Italy
A Giusti, Department of Geriatrics and Muscoloskeletal Sciences, E.O. Galliera Hospital, Genova, Italy
M Boschetti, Department of Internal Medicine, University of Genova, Genova, Italy
M Bovio, Department of Internal Medicine, University of Genova, Genova, Italy
C Teti, Department of Internal Medicine, University of Genova, Genova, Italy
G Leoncini, Department of Internal Medicine, University of Genova, Genova, Italy
D Ferone, Department of Internal Medicine, University of Genova, Genova, Italy
G Murialdo, Department of Internal Medicine, University of Genova, Genova, Italy
F Minuto, Department of Internal Medicine, University of Genova, Genova, Italy
Objectives: Previous studies suggested that vitamin D modulates circulating IGF1. We investigated this effect in adults and its clinical relevance in the management of growth hormone deficiency (GHD).
Design and methods: IGF1 levels were prospectively measured before and after 12 weeks of treatment with oral vitamin D3 (5000 or 7000 IU/week) vs. no intervention in 39 subjects 61.9±7.9 years old. The frequency of IGF1 values ≥ 50th age- and sex-specific percentile in relation to vitamin D status, as determined by the concentration of 25-hydroxyvitamin D [25(OH)D], was retrospectively assessed in 69 GHD patients (57.4±16.6 yr) on stable hormone replacement and with 25(OH)D and IGF1 concurrently measured.
Results: Five-thousand and 7000 IU vitamin D3/week significantly raised 25(OH)D by 12.7±8.4 ng/ml and 13.1±6.5 ng/ml, respectively (both P < 0.001 vs. baseline). In the 7000 IU group IGF1 levels also significantly increased by 31.3±36.7 ng/ml (P = 0.01). Neither 25(OH)D nor IGF1 significantly varied in controls. IGF1 was ≥ 50th percentile more frequently in GHD patients with ≥ 15 ng/ml than < 15 ng/ml 25(OH)D (65.9% vs. 40.0%, P < 0.05). Logistic regression with adjustment for recombinant human (rh) GH dose, vitamin D supplements, gender, use of thyroid hormones, corticosteroids or estrogen/testosterone, and season revealed a significant positive association between ≥ 15 ng/ml 25(OH)D and IGF1 ≥50th percentile (OR 4.4, 95% CI 1.0-18.8, P < 0.05). A significant negative correlation between 25(OH)D concentrations and rhGH dose was found after correcting for age and IGF1 (β - 0.042, P < 0.01), but not after further adjusting for sex, thyroid, adrenal or gonadal replacement, and season (β - 0.037, P = 0.06).
Conclusions: Vitamin D increases circulating IGF1 in adults. As a result, a better vitamin D status may ease the achievement of normal IGF1 values in GHD.
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