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

Authors


Address for correspondence: Dr E Fitzpatrick, Paediatric Liver, GI and Nutrition Centre, King's College Hospital, Denmark Hill, London SE5 9PJ, UK. E-mail: emer.fitzpatrick@kcl.ac.uk

Summary

What is already known on this subject

  • Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in children and the rising prevalence is closely associated with the rise in obesity.
  • Adipokines, inflammatory mediators which arise from adipocytes or inflammatory cells infiltrating fatty tissue, are likely to be involved in the evolution of steatohepatitis from simple steatosis in nonalcoholic fatty liver disease.

What this study adds

  • Certain adipokines are differentially expressed with different severity of disease in paediatric NAFLD.
  • Plasma monocyte chemoattractant protein 1 and resistin decrease with increasing severity of steatohepatitis.
  • Plasma plasminogen activator 1 and monocyte chemoattractant protein 1 are increased in severe fibrotic NAFLD.

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 α 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.

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