Abstract
Objective: We aimed to examine if myeloid leukocyte profiles are associated with metabolic impairment in children and adolescents with obesity, and if sex, age, or race influence this relationship.Methods: 282 children ages 8–17 were evaluated. Predictor measures were absolute neutrophil counts (ANC), absolute monocyte count, monocyte subtypes and C reactive protein (CRP). Outcome variables were waist circumference, fasting glucose and insulin, HOMA-IR, HbA1c (%) and lipid profiles. Pearson correlation coefficients were used to determine associations between predictor and outcome variables. Wilcoxon two-sample tests were used to evaluate differences by sex.Results: CRP (p < 0.0001), ANC (p < 0.0018), and classical monocytes (p = 0.05) were significantly higher in children with obesity. CRP, ANC and classical monocytes showed positive correlations with waist circumference, insulin, HOMA-IR and triglycerides. CRP was positively associated with ANC overall (p = 0.05). ANC demonstrated positive correlation with monocytes (p < 0.001). The associations between predictor and outcome variables were influenced by sex, race, and age.Conclusions: CRP and myeloid leukocyte populations, specifically classical monocytes and neutrophils associate with both body composition and metabolic parameters in children with obesity suggesting that these cells may play a critical role in metabolic impairment. Race, gender and age interactions between monocytes and metabolic parameters were significant.
Highlights
Obesity leads to a low-grade chronic inflammation in which macrophage activation and neutrophil accumulation enhance tissue dysfunction further promoting metabolic disease [1]
We found a positive correlation between %CD14++CD16− monocytes and waist
To understand which inflammatory factors are changed together, we evaluated the associations of Absolute neutrophil count (ANC) and CRP with the different monocyte populations and identified that CRP trended with ANC overall (p = 0.05) (Figure 3)
Summary
Obesity leads to a low-grade chronic inflammation in which macrophage activation and neutrophil accumulation enhance tissue dysfunction further promoting metabolic disease [1]. The net result is the sustained accumulation and activation of adipose tissue macrophages (ATMs) which shift from an anti-inflammatory, and insulin sensitive, phenotype toward a pro-inflammatory, and insulin resistant, phenotype [1, 3] These activated ATMs secrete pro-inflammatory cytokines and chemokines, that magnify recruitment of neutrophils and macrophages, myeloid cells, into the visceral adipose tissue [1, 3,4,5]. This local inflammation subsequently contributes to an insulin resistant environment, and causes metabolic and cardiovascular complications including hyperinsulinemia, impaired glucose tolerance, hypertension, hypertriglyceridemia, and low HDL cholesterol [6]. An inflammatory phenotype is present in other tissues and may lead to metabolic dysfunction starting as early as childhood [1, 7]
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