Abstract
Macrophage infiltration in two subcutaneous adipose tissue depots and systemic low-grade inflammation were studied in post-obese (PO), obese (O), and control (C) subjects. Young males were recruited into PO: (n = 10, weight-loss avg. 26%, BMI: 26.6 ± 0.7, mean ±SEM kg/m2), O: (n = 10, BMI: 33.8 ± 1.0kg/m2) and C: (n = 10, BMI: 26.6 ± 0.6 kg/m2). PO and C were matched by BMI. Blood and abdominal and gluteal subcutaneous adipose tissue were obtained in the overnight fasted state. Plasma concentrations of IL-6 and CRP were higher (p < 0.05) in O than in PO and C, TNF-α was higher (p < 0.05) only in O compared to PO and IL-18 was similar between groups. The number of CD68+ macrophages was higher (p < 0.05) in the gluteal than the abdominal depot, and higher (p < 0.05) in O and PO compared to C in both depots. The content of CD163+ macrophages was similar between depots but was higher (p < 0.05) in PO compared to C and O in the gluteal depot. In post obese men with a long-term sustained weight loss, systemic low-grade inflammation was similar to non-obese controls despite a higher subcutaneous adipose tissue CD68+ macrophage content. Interestingly, the anti-inflammatory CD163+ macrophage adipose tissue content was consistently higher in post obese than obese and controls.
Highlights
Obesity is associated with a chronic low-grade inflammatory state that predisposes to insulin resistance, type 2 diabetes, and cardiovascular disease [1,2,3]
Body fat, and Body mass index (BMI) were higher (p < 0.05) in Obese compared to the two groups (Table 1)
Body fat, and BMI were higher (p < 0.05) in Obese compared to the other groups but similar between Post obese and Control (Table 1)
Summary
Obesity is associated with a chronic low-grade inflammatory state that predisposes to insulin resistance, type 2 diabetes, and cardiovascular disease [1,2,3]. Chronic low-grade inflammation is characterized by elevated systemic levels of inflammatory markers such as C-reactive protein (CRP), interleukin-6 (IL-6), interleukin-18 (IL-18), and tumour necrosis factor-α (TNF-α) [4,5]. The obesity-associated low-grade inflammation is associated with a higher content of macrophages in the adipose tissue of obese compared to lean subjects [6,7,8,9]. Studies have shown that, depending on the stimuli, macrophages can transform into specialized subtypes with different functional properties [10,11]. Evidence from in vitro cell culture studies suggests that polarization into subtypes M1 and M2 may determine macrophage function [12]. M1 or “classically activated” macrophages produce pro-inflammatory cytokines such as IL-6 and TNF-α.
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