The pooled results using random effects model showed that statin use statistically significantly decreased CRP level (SMD= -0.97; 95% CI, -1.10, -0.85; P < 0.001; I<sup>2</sup>: 95.1%), TNF-α (SMD= -1.88; 95% CI, -2.40, -1.38; P < 0.001; I<sup>2</sup>: 97.2%), IL-6 (SMD= -1.67; 95% CI, -1.98, -1.34; P < 0.001; I<sup>2</sup>: 96.5%), and IL-1 concentrations (SMD= -8.35; 95% CI, -10.49, -6.22; P < 0.001; I<sup>2</sup>: 98.4%) among patients with MetS and related disorders.
Pro-inflammatory cytokines related to insulin resistance and MetS in children are tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, IL-1β, interferon gamma, pigment epithelium-derived factor, chemerin, vaspin, and fetuin A. Anti-inflammatory cytokines associated with insulin resistance and MetS in children are leptin, adiponectin, omentin, fibroblast growth factor (FGF)-21, osteocalcin, and irisin.
Transgenic mice expressing human interleukin 37 (IL-37), an anti-inflammatory cytokine of the IL-1 family, are protected against metabolic syndrome when fed a high-fat diet (HFD) containing 45% fat.
Inflammasomes, which are intracellular multi-protein complexes, promote acute and chronic inflammation via interleukin-1β or interleukin-18 maturation, and they are known targets for metabolic syndromes and cancer.
The aim of the study was to evaluate the influence of interaction between SNP of inflammatory genes (encoding interleukin (IL)-6, IL-1β and IL-10) and plasma fatty acids on the odds of MetS, in a population-based cross-sectional study.
IL-1 antagonism in obese individuals with features of the metabolic syndrome leads to a decrease in serum cortisol, salivary cortisol, and ACTH levels along with a reduction in systolic blood pressure and heart rate.
The decrease in IL-1 receptor antagonist expression after weight loss and the strong correlation between the decrease in IL1B expression and the increase in insulin sensitivity suggest a contribution of these genes to insulin-resistant states found in obesity and the metabolic syndrome.
These results suggested that IL1beta genetic variants were associated with measures of chronic inflammation and the MetS risk, and that genetic influences were more evident among subjects with low (n-3) PUFA intake.