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.
Highlights
Obesity is defined as a long-term positive caloric imbalance leading to adipose tissue expansion, which may occur via increases in adipocyte size, number or both [1,2]
The objective of this study was to evaluate the plasmatic levels of adipokines [leptin, adiponectin, resistin, soluble TNF receptors 1 (sTNFR1), sTNFR2 and chemokines (MCP-1, RANTES, IL-8, inducible protein 10 (IP-10) and MIG)] and brain-derived neurotrophic factor (BDNF), serum cortisol and redox status in overweight/obese infants versus normal-weight peers matched for gender, age, socioeconomic status, maternal education, exclusive breastfeeding until 6 months, and the use of vitamin supplements
The leptin levels were positively associated with sTNFR1 levels and negatively associated with adiponectin levels in overweight/ obese infants, showing that the increase in plasma leptin levels can create an environment that predisposes to a subsequent pro-inflammatory response
Summary
Obesity is defined as a long-term positive caloric imbalance leading to adipose tissue expansion, which may occur via increases in adipocyte size (hypertrophy), number (hyperplasia) or both [1,2]. Obese individuals presented a chronic low-grade inflammation that involves excessive adipocyte hypertrophy, immune cell infiltration, extracellular matrix overproduction, increased production of pro-inflammatory adipokines and redox imbalance [3,4,5]. An increase in pro-inflammatory adipokines secreted by infiltrated macrophages and hypertrophied adipocytes, as well as an elevated production of reactive oxygen species (ROS), can decrease the differentiation capacity of preadipocytes and inhibit adipogenesis [4,5,9,10]. Postnatal weight gain in infancy is associated with overweight and obesity, central adiposity, low-grade systemic inflammation and redox imbalance in later childhood, predisposing to metabolic derangements and chronic inflammatory diseases like insulin resistance and cardiovascular impairment [16,17,18]
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