Decrease in Adiponectin Levels Correlates to Growth Response in Growth Hormone-Treated Children

Background/Aims: Adiponectin is secreted by adipose tissue and circulates in human plasma at high levels. Decreased adiponectin levels are associated with insulin resistance and obesity. The aim of this study was to investigate whether changes in serum adiponectin levels are related to the growth re...

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Veröffentlicht in:HORMONE RESEARCH IN PAEDIATRICS 2009-01, Vol.71 (4), p.213-218
Hauptverfasser: Andersson, B., Carlsson, L.M.S., Carlsson, B., Albertsson-Wikland, K., Bjarnason, R.
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Sprache:eng
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Zusammenfassung:Background/Aims: Adiponectin is secreted by adipose tissue and circulates in human plasma at high levels. Decreased adiponectin levels are associated with insulin resistance and obesity. The aim of this study was to investigate whether changes in serum adiponectin levels are related to the growth response, insulin levels and insulin resistance during growth hormone (GH) treatment. Methods: The study included 94 short prepubertal children (19 girls and 75 boys). The mean age at the start of daily GH injections was 9.04 ± 2.38 years. Adiponectin levels in serum were measured using an ELISA. Results: At baseline, adiponectin correlated with the first-year growth response (r = 0.26, p = 0.012). Adiponectin decreased significantly after 1 week, 3 months and 1 year from 14.5 ± 5.71 to 13.1 ± 5.22 (p < 0.0001), 10.3 ± 4.82 (p < 0.0001) and 12.5 ± 5.34 μg/ml (p < 0.0001), respectively. There were significant correlations between the first-year growth response and the decrease in adiponectin levels after 3 months and 1 year (r = –0.38, p < 0.0001 and r = –0.47, p < 0.0001, respectively). No correlations between adiponectin, insulin and the homeostasis model assessment of insulin resistance were seen. Conclusions: GH treatment in prepubertal children decreases serum adiponectin levels, and the decrease is correlated to the growth response. No correlations between adiponectin and insulin levels or insulin resistance were found.
ISSN:1663-2818
0301-0163
1423-0046
1663-2826
1423-0046
DOI:10.1159/000201110