Endocrine Abstracts

Background and aim: Although chronic low-grade inflammation is observed in obese subjects, the underlying mechanisms modulating this process are still unclear. The Comparative Gene Identification-58 (CGI-58) is a lipid droplet-associated protein that has an important role in mediating intracellular fat hydrolysis by acting as a coactivator of the adipose Triglyceride Lipase (ATGL). Recent evidence suggests that CGI-58 also has a role in chronic inflammation and insulin resistance (IR). Accordingly, macrophage specific Cgi-58 knockout aggravated high fat diet-induced inflammation and IR in mice through activation of the NLRP3 inflammasome. However, to date, only few studies have evaluated CGI-58 expression in obese patients, with inconclusive results. Therefore, the aim of this study was to evaluate CGI-58 expression in subcutaneous adipose tissue (SAT) from subjects with different BMI. Methods: SAT was obtained from 67 individuals who undergone bariatric surgery or elective abdominal surgery. Twenty-six patients were classified as having morbid-obesity (BMI ≥40 kg/m²), 27 as having moderate-obesity (BMI: 30.0 – 39.9 kg/m²), and 14 as non-obese subjects (BMI <25 kg/m²). CGI-58 expression was quantified using RT-qPCR technique. Basal metabolic rate (BMR) was measured by indirect calorimetry and body composition variables by dual-energy X-ray absorptiometry. All subjects underwent complete physical and laboratory evaluations. Results: CGI-58 expression was decreased in morbid-obese and moderate-obese patients compared with the non-obese group (median 0.59 (minimum 0.18 – maximum 1.39) vs 0.83 (0.28 – 2.15) vs. 1.70 (0.73 – 3.63) n-fold change; P <0.001). CGI-58 expression was also negatively correlated with BMI (r=−0.432, P <0.001), fat mass (r=−0.380, P=0.003), free fat mass (r=−0.488, P <0.001), and BMR (r=−0.373, P=0.002). Regarding lipid profile, CGI-58 expression negatively correlated with triglycerides (r=−0.585, P <0.001) and cholesterol levels (r=−0.305, P=0.015) while positively correlated with HDL levels (r=0.250, P=0.046). Negative correlations were also found between CGI-58 expression and HbA1c (r=−0.421, P <0.001), insulin levels (r=−0.332, P=0.009) and IR (r=−0.317, P=0.013). Conclusions: CGI-58 gene expression is decreased in obese patients compared to non-obese subjects and is inversely correlated with a worse metabolic profile.