Neuroendocrine Inflammatory Responses in Overweight/Obese Infants

PLoS One. 2016 Dec 1;11(12):e0167593. doi: 10.1371/journal.pone.0167593. eCollection 2016.

Abstract

Childhood obesity is related to a cascade of neuroendocrine inflammatory changes. However, there remains a gap in the current literature regarding the possible occurrence of these changes in overweight/obese infants. The objective of this study was to evaluate adipokines, cortisol, brain-derived neurotrophic factor (BDNF) and redox status in overweight/obese infants versus normal-weight peers. A cross-sectional study was conducted with 50 infants (25 in the overweight/obese group and 25 in the normal-weight group) between 6 and 24 months. Plasma levels of leptin, adiponectin, resistin, soluble tumor necrosis factor (TNF) receptors, chemokines, BDNF, serum cortisol and redox status were measured. Unpaired Student's t-test was used to analyze the results and a probability of p<0.05 was acceptable for rejection of the null hypothesis. The Pearson correlation was used to verify the association between the biomarkers analyzed in each group. Plasma levels of leptin (p = 0.0001), adiponectin (p = 0.0007) and BDNF (p = 0.003), and serum cortisol (p = 0.048) were significantly higher in overweight/obese infants than normal-weight infants. In contrast, the concentration of thiobarbituric acid reactive substances (TBARS) (p = 0.004), and catalase (p = 0.045) and superoxide dismutase activity (p = 0.02) were lower in overweight/obese infants than normal-weight peers. All the results together indicate neuroendocrine inflammatory response changes in overweight/obese infants between 6 and 24 months. Although there is already an environment that predisposes for a subsequent pro-inflammatory response, neuroendocrine secretion changes that permit the control of the inflammatory process in this age interval can be observed.

MeSH terms

  • Adipokines / blood
  • Adiponectin / blood
  • Biomarkers / blood
  • Body Composition
  • Body Weight
  • Brain-Derived Neurotrophic Factor / blood
  • Cross-Sectional Studies
  • Humans
  • Hydrocortisone / blood
  • Infant
  • Inflammation / blood*
  • Inflammation / pathology
  • Leptin / blood
  • Neurosecretory Systems / metabolism*
  • Neurosecretory Systems / pathology
  • Obesity / blood*
  • Obesity / pathology
  • Overweight / blood*
  • Overweight / pathology
  • Oxidation-Reduction

Substances

  • Adipokines
  • Adiponectin
  • Biomarkers
  • Brain-Derived Neurotrophic Factor
  • Leptin
  • BDNF protein, human
  • Hydrocortisone

Grants and funding

This work was supported by the Universidade Federal dos Vales do Jequitinhonha e Mucuri for institutional support, the CNPq, FAPEMIG, and CAPES for financial support and scholarships. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.