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Analysis of circulating insulin-like growth factor-1 (IGF-1) and IGF binding protein-3 (IGFBP-3) in tobacco smokers and non-smokers

BACKGROUND: IGF-1 and the major serum IGF-1 binding protein, IGFBP-3, are under extensive investigation as potential prognostic markers of specific malignancies and vascular diseases. However, there is conflicting evidence that tobacco smoking may influence systemic concentrations of IGF-1 and IGFBP...

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Detalles Bibliográficos
Autores principales: Palmer, RM, Wilson, RF, Coward, PY, Scott, DA
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2002
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2671651/
https://www.ncbi.nlm.nih.gov/pubmed/19570255
http://dx.doi.org/10.1186/1617-9625-1-2-157
Descripción
Sumario:BACKGROUND: IGF-1 and the major serum IGF-1 binding protein, IGFBP-3, are under extensive investigation as potential prognostic markers of specific malignancies and vascular diseases. However, there is conflicting evidence that tobacco smoking may influence systemic concentrations of IGF-1 and IGFBP-3. SUBJECTS AND METHODS: Serum concentrations of IGF-1 and IGFBP-3 were measured in 20 smokers and 20 non-smokers, matched for age and gender. Serum concentrations of cotinine, the major metabolite of nicotine, and ICAM-1, known to exhibit a dose-dependent relationship with cotinine, were also assayed. RESULTS: There was no difference between the systemic concentrations of IGF-1 or IGFBP-3 found in smokers and non-smokers (IGF-1: mean [s.d]; 104 [29] vs 101 [24] ng ml(-1), respectively; and IGFBP-3: 2562 [522] vs 2447 [570] ng ml(-1), respectively). Similarly, there was no correlation between serum cotinine and IGF-1 or IGFBP-3 concentrations in smokers. Soluble ICAM-1 concentrations were significantly increased in smokers, compared to non-smokers (mean [s.d]; 258 [60] vs 194 [50] ng ml(-1), respectively; p = 0.002). CONCLUSION: There was no relationship noted between tobacco smoking and either IGF-1 or IGFBP-3. These data suggest that smoking would not appear to be a major confounder of the reported clinical associations between IGF-1, IGFBP-3, or IGF-1/IGFBP-3 ratios and specific disease entities.