Insulin growth factor I and hypogonadism in cirrhosis

Mezey, Esteban

doi:10.1002/hep.510310333

Cited by 3 publications

(1 citation statement)

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“…Other studies investigated the effect of exogenous IGF-1 application and revealed an improvement in liver function and a reduction in oxidative liver damage and fibrosis [7,16,21,29] . Furthermore, the studies described that, due to its mitogenic, chemotactile and fibrogenic activities, IGF-1 triggers hepatic stellate cells and myofibroblasts to induce mitosis and collagen production, promoting fibroproliferative processes in the injured liver [16,30] . The present study associated laboratory parameters of liver dysfunction to IGF-1 and IGFBP-3 levels.…”

Section: Introductionmentioning

confidence: 98%

IGF-1 and IGFBP-3 in patients with liver disease/IGF-1 und IGFBP-3 bei Patienten mit Lebererkrankungen

Wallek

Friedrich

Ittermann

et al. 2013

Laboratoriumsmedizin

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Background: Hepatic stellate cells are stimulated by insulin-like growth factor 1 (IGF-1) and high IGF-1 levels attenuate fibrogenesis and accelerate liver regeneration. This effect is mainly mediated by upregulation of hepatic growth factor and downregulation of transforming growth factor β 1. Thus, decreased IGF-1 levels in patients point to an impaired regeneration potential in chronic liver failure. The objective of this study was to evaluate the relation between liver dysfunction and levels of IGF-1 and IGFbinding protein 3 (IGFBP-3) levels. Methods: One hundred and twenty-seven patients aged 45 to 60 years (36 women, 91 men) with diagnosed liver disease were recruited for the study. From the Study of Health in Pomerania (SHIP), 508 healthy individuals were matched for age and sex as the control group. Associations between laboratory parameters of liver failure and IGF-1 or IGFBP-3 were examined. Serum IGF-1 and serum IGFBP-3 levels were measured by automated two-site chemiluminescence immunoassays. Results: IGF-1 and IGFBP-3 levels were significantly lower in patients with liver diseases. There was no detectable homogeneous relation between liver transaminases and IGF-1 or IGFBP-3 levels in the patient group alone. Patients with a Child Pugh Score of C revealed lower levels of IGF-1 than patients with Child Pugh Scores of B or A. In IGFBP-3, this association was also apparent, but statistically not significant. In pooled analyses of patients and healthy controls, negative associations between aspartate aminotransferase (ASAT) and γ -glutamyltranspeptidase (GGT) activities and IGF-1 and IGFBP-3 levels, as well as between alanine aminotransferase (ALAT) activity and IGF-1 levels were detected. Conclusions: We demonstrated that compared with healthy controls patients with liver disease exhibited lower IGF-1 and IGFBP-3 levels.

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