Abstract
Elevated soluble cluster of differentiation 163 (sCD163) concentrations, a marker of macrophage activation, are associated with obesity. Weight reduction decreases circulating CD163 levels, and changes in sCD163 levels are associated with improved metabolic dysfunction. Currently, the relationship between sCD163 and diet remains unclear. This study investigated dietary patterns associated with sCD163 concentrations and its predictive effect on metabolic syndrome (MetS). Data on anthropometrics, blood biochemistry, and a food frequency questionnaire were collected from 166 Taiwanese adults. sCD163 levels independently predicted MetS (odds ratio (OR): 5.35; 95% confidence interval (CI): 2.13~13.44, p < 0.001), non-alcoholic fatty liver disease (OR: 2.19; 95% CI: 1.03~4.64, p < 0.001), and central obesity (OR: 3.90; 95% CI: 1.78~8.55, p < 0.001), after adjusting for age and sex. An adjusted linear regression analysis revealed strong correlations between levels of sCD163 and aspartate transaminase (AST) (β = 0.250 (0.023~0.477), p < 0.05) and red blood cell aggregation (β = 0.332 (0.035~0.628), p < 0.05). sCD163-associated dietary pattern scores (high frequencies of consuming noodles and desserts, and eating at home, and a low intake frequency of steamed/boiled/raw food, white/light-green-colored vegetables, orange/red/purple-colored vegetables, dairy products, seafood, dark-green leafy vegetables, and soy products) were positively correlated with MetS, liver injury biomarkers, and sCD163 levels (all p for trend < 0.05). Individuals with the highest dietary pattern scores (tertile 3) had a 2.37-fold [OR: 2.37; 95% CI: 1.04~5.37, p < 0.05] higher risk of MetS compared to those with the lowest scores (tertile 1). Overall, the study findings suggest the importance of a healthy dietary pattern in preventing elevated sCD163 levels and diet-related chronic disease such as MetS.
Highlights
Substantial evidence has demonstrated a positive relationship between circulating soluble cluster of differentiation 163 concentrations and obesity-related comorbidities such as diabetes, non-alcoholic fatty liver disease (NAFLD), and metabolic syndrome (MetS) [1,2].CD163 is a transmembrane scavenger receptor mainly expressed on monocyte-macrophage cell lineages
The predictive effect of soluble cluster of differentiation 163 (sCD163) levels on MetS remained significant after further adjusting for body mass index (BMI) (OR: 4.62; 95% confidence interval (CI): 1.58~13.51, p = 0.005)
This result is in line with a recent study investigating the association between the risk of obesity and at-home and away-from-home dietary patterns among Brazilian adolescents, which found that an unhealthy dietary pattern consumed at home was associated with an increased risk of obesity, while the away-from-home food consumption frequency was not [25]. Similar to their findings [25], the present study found that participants who preferred to eat at home were more likely to have a Western dietary pattern and highlights the need to improve food choices when individuals prefer to eat at home
Summary
Substantial evidence has demonstrated a positive relationship between circulating soluble cluster of differentiation 163 (sCD163) concentrations and obesity-related comorbidities such as diabetes, non-alcoholic fatty liver disease (NAFLD), and metabolic syndrome (MetS) [1,2].CD163 is a transmembrane scavenger receptor mainly expressed on monocyte-macrophage cell lineages. The CD163 surface receptor is shed as a soluble form by a metalloproteinase-dependent pathway, a mechanism that involves cleavage of tumor necrosis factor (TNF)-α [3]. Other factors such as a high-fat diet, lipopolysaccharides, and endoplasmic reticular stress can trigger CD163+ macrophage activation and the release of sCD163 [4,5,6]. It was found that circulating CD163 is positively correlated with messenger (m)RNA expression of CD163 in adipose tissues, and circulating CD163, and adipose CD163 mRNA levels are correlated with the glucose disposal rate [7]. SCD163 levels might reflect the degree of macrophage infiltration into adipose tissues and the ability of adipocytes to utilize glucose
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