IGF1 concentrations have been reported to increase with 25-hydroxyvitamin D (25(OH)D) values in population studies, but it is unclear whether this association expresses a cause-effect relationship. Mice genetically deficient of steroid receptor coactivator 3, a transcriptional coactivator for the nuclear vitamin D receptor, have significantly lower circulating IGF1 levels than wild-types.
We measured serum fasting 25(OH)D and IGF1 by enzyme- and radioimmunoassay, respectively, in 42 internal medicine outpatients, aged 61.7±8.9 years, at follow-up visits for stable or recovering medical conditions. The study was performed in Genova, Italy, at latitude 44° North, over Spring and Summer.
Mean (±S.D.) 25(OH)D and IGF1 concentrations were 15.7 (±9.1) ng/ml and 182.6 (±77.8) ng/ml respectively. There was a positive correlation between 25(OH)D and IGF1 values (r 0.33, P<0.05).
To understand in principle whether vitamin D status does affect GH/IGF1 axis, in 20 patients we measured 25(OH)D, IGF1, and GH (the latter by immunoradiometric assay) before and after 12 weeks of 5000 IU cholecalciferol/week (six subjects), 7000 IU cholecalciferol/week (seven subjects), or no treatment (controls, seven subjects). A significant increase in serum 25(OH)D was observed after supplementation with both cholecalciferol dosages (+16.217.7 ng/ml vs baseline, P<0.01). Nonsignificantly higher GH levels were also found after either cholecalciferol dose (+1.171.19 mIU/l). Seven thousands, but not 5000 IU/week significantly raised IGF1 concentration of 41.1 ng/ml (P<0.05 vs baseline).
A significant increase in 25(OH)D values of 7.8 ng/ml vs baseline (P<0.05) was also observed in controls after 12 weeks, likely because of sun exposure during normal outdoor life. GH and IGF1 levels did not change significantly.
These preliminary results suggest that treatment with at least 1000 IU/day vitamin D results in increased circulating IGF1, and that the relationship between 25(OH)D and IGF1 concentrations described in cross-sectional analyses may be causal.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.
05 - 09 May 2012
European Society of Endocrinology