Dectin-1 as a Potential Inflammatory Biomarker for Metabolic Inflammation in Adipose Tissue of Individuals with Obesity

Abstract

In obesity, macrophage activation and infiltration in adipose tissue (AT) underlie chronic low-grade inflammation-induced insulin resistance. Although dectin-1 is primarily a pathogen recognition receptor and innate immune response modulator, its role in metabolic syndromes remains to be clarified. This study aimed to investigate the dectin-1 gene expression in subcutaneous AT in the context of obesity and associated inflammatory markers. Subcutaneous AT biopsies were collected from 59 nondiabetic (lean/overweight/obese) individuals. AT gene expression levels of dectin-1 and inflammatory markers were determined via real-time reverse transcriptase-quantitative polymerase chain reaction. Dectin-1 protein expression was assessed using immunohistochemistry. Plasma lipid profiles were measured by ELISA. AT dectin-1 transcripts and proteins were significantly elevated in obese as compared to lean individuals. AT dectin-1 transcripts correlated positively with body mass index and fat percentage (r ≥ 0.340, p ≤ 0.017). AT dectin-1 RNA levels correlated positively with clinical parameters, including plasma C-reactive protein and CCL5/RANTES, but negatively with that of adiponectin. The expression of dectin-1 transcripts was associated with that of various proinflammatory cytokines, chemokines, and their cognate receptors (r ≥ 0.300, p ≤ 0.05), but not with anti-inflammatory markers. Dectin-1 and members of the TLR signaling cascade were found to be significantly associated, suggesting an interplay between the two pathways. Dectin-1 expression was correlated with monocyte/macrophage markers, including CD16 , CD68 , CD86 , and CD163 , suggesting its monocytes/macrophage association in an adipose inflammatory microenvironment. Dectin-1 expression was independently predicted by CCR5 , CCL20 , TLR2 , and MyD88 . In conclusion, dectin-1 may be regarded as an AT biomarker of metabolic inflammation in obesity.

Adipose Tissue Caveolin-1 Upregulation in Obesity Involves TNF-α/NF-κB Mediated Signaling

“…The exclusion criteria were as follows: individuals with a history of chronic disease or medications, malignancy, and pregnancy. Anthropometric measurements, such as height, weight, and waist circumference, were measured, as described previously [ 20 , 21 ]. Whole-body compositions including body fat percentage, soft lean mass, and total body water were measured using an IOI 353 Body Composition Analyzer (Jawon Medical, Seoul, Republic of Korea).…”

Standardized Sanguisorba officinalis L. Extract Inhibits Adipogenesis and Promotes Thermogenesis via Reducing Oxidative Stress

“…The avidin-biotin complex (ABC) method was utilized for immunohistochemistry. In brief, according to previously described methods [ 28 , 29 ], deparaffinized and hydrated sections were reacted with 0.3% hydrogen peroxide (in 100 mM phosphate-buffered saline, pH 7.4) for 20 min at room temperature. After that, the sections were immersed into 5% normal goat, rabbit, or horse serum (Vector Laboratories Inc., Burlingame, CA, USA) for 30 min at room temperature.…”

Expression of Steroid Receptor RNA Activator 1 (SRA1) in the Adipose Tissue Is Associated with TLRs and IRFs in Diabesity

“…Briefly, 50 ng of cDNA was amplified using TaqMan Gene Expression Master Mix (Applied Biosystems, CA, USA) and gene-specific 20 X TaqMan gene expression assays including forward and reverse primers ( Supplementary Table S2 ), target-specific TaqMan 5′FAM-labeled and 3′NFQ-labeled MGB probe, using 7500 Fast Real-Time PCR System (Applied Biosystems, CA, USA) as described elsewhere [ 42 ]. Target gene expression relative to control (NW fat samples) was determined using comparative Ct method [ 47 ] and data were normalized to GAPDH gene expression as described [ 48 , 49 , 50 , 51 , 52 ].…”