Analysis of adipokine concentrations in paediatric non-alcoholic fatty liver disease

被引:38
作者
Fitzpatrick, E. [1 ]
Dew, T. K. [2 ]
Quaglia, A. [3 ]
Sherwood, R. A. [2 ]
Mitry, R. R. [3 ]
Dhawan, A. [1 ]
机构
[1] Kings Coll London, Sch Med, Paediat Liver GI & Nutr Ctr, London WC2R 2LS, England
[2] Kings Coll Hosp London, Dept Clin Biochem, London SE5 9PJ, England
[3] Kings Coll London, Sch Med, Inst Liver Studies, London WC2R 2LS, England
来源
PEDIATRIC OBESITY | 2012年 / 7卷 / 06期
关键词
Adipokines; biomarkers; non-invasive; paediatric non-alcoholic fatty liver disease; steatohepatitis; PLASMINOGEN-ACTIVATOR INHIBITOR-1; SERUM LEPTIN LEVELS; INSULIN-RESISTANCE; ADIPOSE-TISSUE; ADIPONECTIN RECEPTORS; GENE-EXPRESSION; OBESITY; STEATOHEPATITIS; INFLAMMATION; PATHOGENESIS;
D O I
10.1111/j.2047-6310.2012.00082.x
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Background: Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in children. It is important to distinguish children with more severe disease or steatohepatitis (NASH) from those with the less severe simple steatosis (SS) as prognosis differs. The importance of adipokines in the evolution of NASH is well recognized. Objective: As adipokines are important in mediating inflammation, they may also be useful biomarkers of disease. Methods: Plasma from 40 children (30 boys), median age 13.4 years, with liver biopsy-proven NAFLD was analysed. Liver biopsies were scored using the NAFLD activity score and compared with adipokine concentrations. Results: Median body mass index z-score was 2.12 with a median homeostasis model of assessment-insulin resistance of 4.08. Resistin was lower in NASH than in SS (P = 0.03). Monocyte chemoattractant protein 1 (MCP-1) was also lower in NASH (P = 0.04). MCP-1 was higher in children with severe fibrosis (P = 0.008) with an area under the receiver operating characteristic curve (AUROC) of 0.76. Plasminogen activator inhibitor 1 (PAI-1) was also higher in this group (P = 0.011) with an AUROC of 0.78. There were no significant differences in leptin, adiponectin, adipsin, interleukin (IL) 6, IL10 or tumour necrosis factor a between groups. Conclusion: PAI-1 MCP-1 and resistin were differentially expressed with increasing severity of NAFLD. Though it is unlikely that this profile alone would serve as a biomarker of disease, differences found may contribute to understanding the role of these mediators in NAFLD.
引用
收藏
页码:471 / 479
页数:9
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