Gastrointestinal inflammation and the circulating IGF system in humans

Ivona Baricevic-Jones, Ivona I. Baričević, D. R. Jones, J. A. Nikolić, O. Nedić

    Research output: Contribution to journalArticlepeer-review


    Insulin-like growth factors (IGFs) and their binding proteins (IGFBPs) have important anabolic functions in normal tissue growth, which in excess may lead to tumorigenesis. In the present study, circulating IGF-I, IGF-II and their binding proteins (IGFBP-3, IGFBP-2 and IGFBP-1) were determined in 92 adult patients with gastrointestinal inflammation (Crohn's disease, colitis ulcerosa, gastritis, duodenitis errosiva, gastrointestinal candidiasis, and rotaviral and adenoviral enteritis). Serum IGF concentrations were measured by radioimmunoassay, while IGFBP profiles and IGFBP proteolytic patterns were characterized by immunoblotting. Concentrations of both IGF-I and IGF-II were significantly (p <0.001) lower in patients than in healthy subjects. Immunoblotting demonstrated a decreased amount of intact IGFBP-3 (by approximately 60%), whereas 1GFBP-2 and IGFBP-1 were increased (approximately 1.7 and 3.5-fold, respectively). No alteration in either fragmentation pattern or relative degree of proteolysis was detected in patients compared to the control group. It may be concluded that the IGF system is seriously imbalanced in patients with gastrointestinal inflammation, regardless of primary cause. These findings may help towards a better understanding of the metabolic outcome of the inflammatory process, and possibly in predicting the efficiency of patient recovery. © Georg Thieme Verlag.
    Original languageEnglish
    Pages (from-to)22-27
    Number of pages5
    JournalHormone and Metabolic Research
    Issue number1
    Publication statusPublished - Jan 2006


    • Gastrointestinal tract
    • IGF
    • IGFBP
    • Inflammation
    • Proteolysis


    Dive into the research topics of 'Gastrointestinal inflammation and the circulating IGF system in humans'. Together they form a unique fingerprint.

    Cite this