By H. P. F. Koppeschaar, Torsten Tuvemo, Peter Trainer, Philip Zeitler
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Extra resources for 38th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: Granada, Spain, April 7-8, 2006 (Hormone Research)
Over the first 6 months of life, there is a gradual induction of GH-regulated growth that coincides with the appearance of growth hormonebinding protein in the circulation [23, 24], and by 18 months of age, linear growth is largely regulated through the GH/IGF-I axis. During childhood, serum GH and IGF-I levels continually rise, but with the onset of puberty, there is a dramatic increase in GH pulse amplitude with a concomitant increase in IGF-I generation that peaks at 1 year after peak height velocity [25–28].
12 Jørgensen JOL: Human growth hormone replacement therapy: pharmacological and clinical aspects. Endocr Rev 1991; 12: 189– 207. 13 Gotherstrom G, Svensson J, Koranyi J, Alpsten M, Bosaeus I, Bengtsson B, Johannsson G: A prospective study of 5 years of GH replacement therapy in GH-deficient adults: sustained effects on body composition, bone mass, and metabolic indices. J Clin Endocrinol Metab 2001;86:4657–4665. , USA Key Words Growth hormone ؒ Insulin-like growth factor I ؒ Growth hormone deficiency ؒ Insulin sensitivity ؒ Insulin secretion Abstract Background: The increased risk for development of type 2 diabetes mellitus (T2DM) in adults with growth hormone deficiency (GHD) has been attributed to insulin resistance arising from increased visceral fat accumulation and the putative effects of low insulin-like growth factor I (IGF-I) levels on pancreatic ␤-cell mass and insulin secretion.
1 mg/day are both physiological and more efficacious in improving glucose metabolism than standard GH doses titrated to normalise serum IGF-I levels. Low GH doses induced modest increments in free IGF-I without promoting lipolysis and thus contributed Horm Res 2007;67(suppl 1):37–42 39 to the beneficial effects on postabsorptive insulin sensitivity. However, it is yet to be determined whether ␤-cells are able to recover in patients with GHD, and risk for T2DM may persist even with low-dose therapy.