Endocrine

, Volume 43, Issue 2, pp 412–418

Insulin-like growth factor I, growth hormone, and insulin sensitivity: the effects of a one-year cholecalciferol supplementation in middle-aged overweight and obese subjects

Authors

    • Department of MedicineUniversity Hospital of North Norway
    • Endocrine Research Group, Institute of Clinical MedicineUniversity of Tromsø
  • Vivian Berg
    • Department of Laboratory MedicineUniversity Hospital of North Norway
  • Rolf Jorde
    • Endocrine Research Group, Institute of Clinical MedicineUniversity of Tromsø
Original Article

DOI: 10.1007/s12020-012-9825-6

Cite this article as:
Kamycheva, E., Berg, V. & Jorde, R. Endocrine (2013) 43: 412. doi:10.1007/s12020-012-9825-6

Abstract

Both altered GH-IGF-I axis and low serum levels of 25-hydroxyvitamin D (25(OH)D) are linked to measures of metabolic syndrome. Our hypothesis was that there is a relation between GH, IGF-I, and 25(OH)D; and that vitamin D supplementation may have an effect on the levels of GH, IGF-I, and IGF-I/IGFBP-3 ratio. 318 overweight and obese subjects completed a one-year randomized intervention with either 40,000 or 20,000 IU cholecalciferol per week or placebo. GH, IGF-I, IGFBP-3 and measures of insulin resistance were evaluated at baseline and at the end of study. There was a significant relation between entities of GH-IGF-I axis and insulin resistance. Subjects with severe obesity had significantly lower serum 25(OH)D and had a significant linear decline in IGF-I/IGFBP-3 ratio with increasing serum 25(OH)D quartiles. Vitamin D status was an independent predictor of GH-IGF-I axis and supplementation with vitamin D decreased IGF-I/IGFBP-3 ratio in subjects without severe obesity. No corresponding effect of vitamin D supplementation on BMI or insulin resistance was observed. Adverse effects of GH-IGF-I axis on glucose metabolism and the development of metabolic syndrome may be in part associated with the changes in vitamin D status.

Keywords

Growth hormone IGF-I Vitamin D Obesity Insulin resistance

Copyright information

© Springer Science+Business Media New York 2012