- Meeting abstract
- Open Access
Evaluation of NLRP3 inflamassome expression and its endogen inhibitor CGI-58 in subjects with different obesity degrees
© Rheinheimer et al. 2015
- Published: 11 November 2015
- Basal Metabolic Rate
- NLRP3 Gene
- NLRP3 Activity
- Glycemic Profile
- NLRP3 Expression
Obesity is associated with a state of low-grade chronic inflammation, commonly causing insulin resistance (IR) and type 2 diabetes mellitus (T2D). The NLRP3 inflamassome is a key mediator of metabolic inflammation, and it has been shown to be activated in macrophages of newly diagnosed insulin resistant-T2D patients. In humans, reduction in NLRP3 expression in adipose tissue is linked to decreased inflammation and improved insulin sensitivity in obese T2D patients. Recently, it was demonstrated that the lipolytic factor CGI-58 is an endogenous suppressor of NLRP3 activity in animal models. Therefore, the aim of this study was to evaluate CGI-58 and NLRP3 gene expressions in adipose tissue from individuals with different obesity degrees and their association with metabolic variables.
Subcutaneous adipose tissue was obtained from 35 individuals who undergone bariatric surgery. All individuals underwent a clinical and laboratory evaluation after signing an informed consent form. Fifteen individuals were classified as having morbid-obesity (body mass index (BMI) ≥ 40 kg/m2) and 20 as having moderate-obesity (BMI: 30.0 – 39.9 kg/m2). Gene expressions of CGI-58 and NLRP3 were evaluated using RT-qPCR technique.
The two analyzed groups were similar regarding homeostasis model assessment-IR (HOMA-IR), basal metabolic rate, and lipid and glycemic profile (all P >0.05). NLRP3 expression seems to be increased in morbid-obese patients as compared to the moderate-obesity group, although this difference did not reach formal statistical significance (1.44 (0.38 – 4.11) vs. 0.72 (0.31 – 3.60), P=0.058). In contrast, CGI-58 expression seems to be decreased in morbid-obese patients (0.47 (0.19 – 1.33) vs. 0.70 (0.28 – 2.15), P=0.070). Interestingly, we observed a positive correlation between NLRP3 expression and triglyceride levels (r=0.685, P=0.001). No significant correlations were observed between CGI-58 and NLRP3 expressions and HOMA-IR (P >0.05)
Our preliminary results suggest that NLRP3 and CGI-58 gene expressions are different between morbid-obese and moderate-obese patients. Moreover, our data indicating that NLRP3 expression is correlated with triglycerides is in agreement with studies showing an effect of diet on NLRP3 regulation.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.