Abstract
Obesity results from excess energy intake over expenditure and is characterized by chronic low-grade inflammation involving circulating monocytes (Mo) and group 2 innate lymphoid cells (ILC2s) imbalance. We analyzed circulating Mo subsets and ILC2s percentages and β2-adrenergic receptor (β2AR) expression in lean and obese subjects, and the possible effect of hypocaloric restriction on these innate immune cells. In 139 individuals aged 45 to 57 years, classified in 74 lean individuals (>18.9kg/m2 BMI <24.9kg/m2) and 65 with obesity (n = 65), we collected fasting blood samples to detect Mo subsets, ILC2s number, and β2AR expression by flow cytometry. Lipids, insulin, leptin, and acylated-ghrelin concentrations were quantified. Resting energy expenditure (REE) was estimated by indirect calorimetry. These measurements were repeated in obese subjects after 7-weeks of hypocaloric restriction. Non-classical monocytes (NCM) and β2AR expression on intermediate Mo (IM) were increased in obese individuals (p<0.001, in both cases), whereas the percent of ILC2s was decreased (p<0.0001). Stepwise regression analysis showed significantly negative associations of ILC2s with caloric intake, β2AR expression on IM with REE, but a positive relationship between NCM and HOMA-IR. Caloric restriction allowed a significant diminution of NCM and the β2AR expression on IM, as well as, an increase in the percent of classical Mo (CM), and ILC2s. ΔREE was related to ΔCD16+/CD16- ratio. These findings show that in obesity occur changes in NCM, ILC2s and β2AR expression, which contribute to the low-grade inflammation linked to obesity and might revert with caloric restriction.
Highlights
In obesity, the imbalance of energy intake/expenditure favors the accumulation of fat [1], usually with chronic low-grade inflammation [2], which has effects on energy metabolism at central and peripheral levels
These findings show that in obesity occur changes in Non-classical monocytes (NCM), ILC2s and β2-adrenergic receptor (β2AR) expression, which contribute to the low-grade inflammation linked to obesity and might revert with caloric restriction
We examined factors associated with monocyte subsets percent, ILC2s percent, and β2AR expression using multiple forward stepwise regression analysis testing as candidate regressors: Resting energy expenditure (REE), BMI, mean arterial tension, HDL-C, non-HDL-C, triglycerides, acylated-ghrelin, leptin, HOMA-IR, and caloric intake values; and as confounding factors: gender and age
Summary
The imbalance of energy intake/expenditure favors the accumulation of fat [1], usually with chronic low-grade inflammation [2], which has effects on energy metabolism at central and peripheral levels. In white adipose tissue (WAT) from obese subjects change immune cell composition and function with an effect on energy expenditure. Excessive visceral fat accumulation causes adipose tissue dysfunction that leads to chronic-low grade inflammation with adipocyte hypertrophy and hyperplasia, shift from a type 2 to type 1 cytokine-associated inflammatory environment, altered secretion of adipokines (leptin, adiponectin, and other), and changes in proportions and kind of immune cells toward pro-inflammatory monocytes and Th17 lymphocytes, which strongly contributes to obesity-related comorbidities [3,4,5]
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