Association between serum YKL-40 level and dysglycemia in cystic fibrosis

被引:8
作者
Bouvet, Guillaume F. [1 ]
Maignan, Maxime [2 ]
Arslanian, Elizabeth [1 ]
Coriati, Adele [1 ]
Rabasa-Lhoret, Remi [1 ]
Berthiaume, Yves [1 ]
机构
[1] IRCM, Montreal, PQ H2W 1R7, Canada
[2] Grenoble Univ Hosp, Emergency Dept, F-38043 Grenoble, France
关键词
Cystic fibrosis related diabetes; YKL-40; protein; Dysglycemia; Interleukin-8; Botnia clamp; ENDOTHELIAL DYSFUNCTION; INSULIN-SECRETION; DIABETES-MELLITUS; INFLAMMATION; MARKER; DISEASE; BIOMARKER; PLASMA; LUNG;
D O I
10.1016/j.cyto.2014.10.017
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background: YKL-40, a chitinase-like protein, is a biomarker for type 1 and type 2 diabetes prognosis. We hypothesized that YKL-40 protein levels are elevated in CF patients with dysglycemia. Methods: Seventeen healthy control subjects and 66 CF patients were prospectively recruited and subjected to an oral glucose tolerance test. In all participants, fasting serum YKL-40 was compared between control and CF patients and between normal glucose-tolerant patients (NG-CF) and CF patients with dysglycemia (DG-CF). A Botnia clamp procedure was performed on a subset of patients for each group to determine the impact of acute increases of either glucose or insulin on YKL-40 concentration. Results: CF patients had higher serum YKL-40 values than the controls (113 [49;288] vs. 38 [30;50] ng/ml, p < 0.001). YKL-40 concentrations in CF patients were mainly increased in the DG-CF group, who had significantly higher values: 213 [93;383] vs. 67 [27;97] ng/ml in the NG-CF group, p < 0.001). No significant modulation of YKL-40 concentration was observed in serum of CF (NG or DG-CF) or non-CF patients, after acute exposure to glucose or insulin. Conclusions: Higher serum YKL-40 levels in CF patients are significantly associated with dysglycemia. The increase in YKL-40 is potentially associated with an inflammatory response resulting from chronic glucose intolerance or CF disease evolution. (C) 2014 Published by Elsevier Ltd.
引用
收藏
页码:296 / 301
页数:6
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