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Submitted on September 1, 2006
Accepted on March 21, 2007
Center for Eating Disorders & Dept. of Endocrinology, Odense University Hospital, DK-5000 Odense, Denmark; Medical Research Laboratories, Clinical Institute, Aarhus University, Hospital, DK-8000 Aarhus C, Denmark
* To whom correspondence should be addressed. E-mail: rene.k.stoving{at}dadlnet.dk.
Context: Regulation of IGF-I activity appears crucial in anorexia nervosa (AN) during adaptation to chronic starvation as well as during the regenerative processes upon nutritional restoration.
Objective: To examine the relationship between IGF-I bioactivity and IGF-binding capacity as expressed as formation of the binary complex of IGF - binding protein-1 (IGFBP-1) and IGF-I in patients with AN at different stages and with different subtypes of the disease.
Design: Longitudinal.
Setting: A clinical research center at a university hospital.
Study Participants: We studied a total of 45 women with AN and 24 age-comparable healthy controls.
Main Outcome Measures: IGF-I bioactivity was determined using an IGF-I receptor activation assay, and IGF-I:IGFBP-1 complex formation was determined by an assay, which allows direct determination of the binary complex.
Results: IGF-I bioactivity was significantly decreased in serum from patients with AN. We found significant correlations between total, ultrafiltered free, and bioactive IGF-I. Despite increased IGFBP-1 concentrations, levels of IGF-I/IGFBP-1 binary complex were not significantly increased in AN. Oral contraceptives were associated with increased levels of IGF-I, IGFBP-1 and binary complex formation. Ghrelin levels were only significantly raised in those patients, who had lost more than 5% of the body weight during the last 4 weeks, whereas ghrelin levels in weight stable as well as in weight gaining patients did not significantly differ from the controls.
Conclusions: Total IGF-I level is a suitable marker of IGF-I bioactivity in emaciated patients with AN irrespective of the clinical subtype and acute nutritional state.
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