Literature DB >> 25532040

Residual β-cell function and the insulin-like growth factor system in Danish children and adolescents with type 1 diabetes.

Jesper S Sorensen1, Niels H Birkebaek, Mette Bjerre, Flemming Pociot, Kurt Kristensen, Anne Soee Hoejberg, Jan Frystyk.   

Abstract

CONTEXT: C-peptide-positive adults with type 1 diabetes (T1D) have higher circulating total and free IGF-1 and lower IGF binding protein 1 (IGFBP-1) than C-peptide-negative patients. Whether this is also the case in children remains unknown.
OBJECTIVE: The objective of the study was to examine the IGF system in children/adolescents with and without residual β-cell function (RBF). DESIGN AND PATIENTS: This was a cross-sectional study containing 136 prepubertal (hereof 15 RBF positive) and 206 pubertal (hereof 42 RBF positive) children/adolescents with T1D for 3-6 years as well as 40 prepubertal and 30 pubertal healthy controls. RBF was evaluated by meal-stimulated C-peptide. MAIN OUTCOME MEASURES: Fasting serum levels of bioactive IGF (ie, the ability of serum to activate the IGF-1 receptor in vitro), total IGF-1, total IGF-2, and IGFBP-1 and -3.
RESULTS: Irrespective of pubertal status, patients with T1D showed lower bioactive IGF and total IGF-1, but higher IGFBP-1 as compared with controls (P < .05). When stratified according to RBF status, a positive RBF was associated with normalization of all IGF-related peptides but IGFBP-1 in prepubertal children (P < .05), whereas none of the IGF components were normalized in prepubertal, RBF-negative children. In pubertal children, total IGF-1 and bioactive IGF remained subnormal and IGFBP-1 supranormal, irrespective of RBF status (P < .05).
CONCLUSION: Independent of pubertal status, T1D was associated with an abnormal IGF system. However, a positive RBF status appeared important but only in prepubertal children, in whom all IGF components but IGFBP-1 were normalized. We speculate that the pubertal GH surge induces insulin resistance, which overrides the stimulatory effect that an RBF may exert on the liver-derived IGF system.

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Year:  2014        PMID: 25532040     DOI: 10.1210/jc.2014-3521

Source DB:  PubMed          Journal:  J Clin Endocrinol Metab        ISSN: 0021-972X            Impact factor:   5.958


  8 in total

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4.  Mutations in pregnancy-associated plasma protein A2 cause short stature due to low IGF-I availability.

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  8 in total

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