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Fasting and postprandial markers of inflammation in lean and overweight children

Jessica A Alvarez1, Paul B Higgins, Robert A Oster

  • 1Department of Nutrition Sciences, General Clinical Research Center, University of Alabama at Birmingham, Birmingham, AL 35249, USA. jalvar2@uab.edu

The American Journal of Clinical Nutrition
|February 13, 2009
PubMed

Insights

Excess body fat in children is linked to higher inflammation markers. Central adiposity may influence the body's inflammatory response after meals, suggesting a connection between obesity and inflammation in children.

Area of Science:

  • Pediatric Endocrinology
  • Obesity Research
  • Inflammation Biology

Background:

  • Overweight children exhibit elevated circulating markers of inflammation (MOI) compared to lean children.
  • The influence of adiposity on postprandial MOI responses in children remains unclear.

Purpose of the Study:

  • To investigate the relationship between fasting and postprandial MOI and total/regional adiposity in children.
  • To evaluate the association of MOI with insulin sensitivity in pediatric subjects.

Main Methods:

  • Assessed C-reactive protein (CRP), interleukin-6 (IL-6), and soluble tumor necrosis factor receptor-2 (sTNF-R2) in 59 children (aged 7-12 years) fasting and post-meal.
  • Evaluated insulin sensitivity, body composition, and abdominal adipose tissue distribution using specialized tests (IV-GTT, DXA, CT).

Main Results:

  • Central adiposity measures were not independently linked to fasting MOI.
  • Inverse associations were found between central adiposity and postprandial sTNF-R2 (r = -0.30 to -0.37, P = 0.02-0.006).
  • A near-significant inverse association was observed between intra-abdominal adipose tissue and postprandial CRP (r = -0.27, P = 0.05).

Conclusions:

  • Excess adiposity in children is associated with both fasting and postprandial MOI.
  • Central adiposity may play a role in modulating the postprandial inflammatory response in children.
  • The positive association between insulin sensitivity and IL-6 requires further investigation.
Abstract

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