The Journal of Pediatrics
Volume 147, Issue 6 , Pages 835-838, December 2005

Decreased Serum Adiponectin: An Early Event in Pediatric Nonalcoholic Fatty Liver Disease

From the Division of Gastroenterology and the Department of Pediatrics, University of Louisville, University of Louisville Medical Center, and the Louisville Veterans Administration Medical Center, Louisville, Ky

Received 24 November 2004; received in revised form 10 May 2005; accepted 20 July 2005.

Objective

To evaluate the relative concentrations of cytokines in pediatric nonalcoholic fatty liver disease (NAFLD).

Study design

Thirty children were evaluated at a fasting morning visit to a pediatric research unit.

Results

Compared with normal-weight children (n = 12) and children who were overweight (n = 11), children who had presumed NAFLD (elevated Alanine aminotransferase [ALT] with negative work-up) (n = 7) had significantly lower mean serum adiponectin levels (P = .004). Adiponectin negatively correlated with body mass index (r = −0.60, P = .001), insulin (r = −0.74, P < .001), glucose (r = −0.52, P = .004), and ALT (r = −0.53, P = .003). There was no difference between normal-weight, obese, and presumed NAFLD subjects in mean serum tumor necrosis factor α and interleukin-6 and -8 concentrations nor in tumor necrosis factor α and interleukin-8 and -10 levels in an ex vivo lipopolysaccharide-stimulated system.

Conclusions

Serum adiponectin is reduced in children with elevated ALT, similar to adults. However, children with presumed NAFLD do not have elevated pro-inflammatory cytokine levels. This suggests that depressed adiponectin plays a more proximal role than elevated levels of circulating pro-inflammatory cytokines in the development of NAFLD in children.

ALT, Alanine Amino transferase, BMI, Body mass index, CRP, C-reactive protein, ELISA, Enzyme-linked immunosorbent assay, IL-6, Interleukin-6, IL-8, Interleukin-8, IL-10, Interleukin-10, LPS, Lipopolysaccharide, NAFLD, Nonalcoholic fatty liver disease, NASH, Nonalcoholic steatohepatitis, TNF-α, Tumor necrosis factor-α

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 Supported by American College of Gastroenterology, National Institutes of Health grants AA010762, AA010496, AA013170, and HD048019, a Kentucky Science and Engineering Foundation grant, and the Department of Veterans Affairs.

PII: S0022-3476(05)00707-9

doi:10.1016/j.jpeds.2005.07.030

The Journal of Pediatrics
Volume 147, Issue 6 , Pages 835-838, December 2005