Association between inflammatory markers and non-alcoholic fatty liver disease in obese children

Yamei Duan1, Jiayou Luo1, Xiongfeng Pan1

  • 1Department of Maternal and Child Health, Xiangya School of Public Health, Central South University, Changsha, Hunan, China.

Frontiers in Public Health
|December 19, 2022
PubMed

Insights

Interleukin (IL)-1β, IL-6, and IL-17 are significantly associated with non-alcoholic fatty liver disease (NAFLD) in obese children. These inflammatory markers show promise as non-invasive indicators for NAFLD development.

Area of Science:

  • Pediatrics
  • Hepatology
  • Immunology

Background:

  • Non-alcoholic fatty liver disease (NAFLD) is prevalent in obese children.
  • Non-invasive diagnostic markers for pediatric NAFLD are limited.
  • Exploring inflammatory markers is crucial for early detection and management.

Purpose of the Study:

  • To investigate the association between specific inflammatory markers and NAFLD in obese children.
  • To evaluate the potential of these markers as non-invasive indicators of NAFLD.
  • To identify novel diagnostic or therapeutic targets for pediatric NAFLD.

Main Methods:

  • A case-control study was conducted with 267 obese children (176 with NAFLD, 91 controls).
  • Inflammatory cytokines were measured using enzyme-linked immunosorbent assay (ELISA).
  • Multivariable logistic regression and receiver operating characteristic (ROC) curve analyses were performed.

Main Results:

  • Increased levels of interleukin (IL)-1β, IL-6, and IL-17 were significantly associated with NAFLD.
  • IL-8, IL-12, IL-21, IL-32, TNF-α, NLR, PLR, LMR, MPV, and PDW showed no significant association.
  • The areas under the ROC curves (AUCs) for IL-1β, IL-6, and IL-17 were high (0.94, 0.94, and 0.97, respectively).

Conclusions:

  • IL-1β, IL-6, and IL-17 are significantly associated with NAFLD in obese children.
  • These cytokines may serve as valuable non-invasive biomarkers for NAFLD.
  • Findings suggest potential for novel therapeutic strategies targeting these inflammatory pathways.
Abstract