Among the three groups, leptin, and leptin: adiponectin ratio, and IL-6 levels were highest in MetS, and levels in Obese were greater than Control (p>0.05).
LTA, TNF-alpha, and IL-6 genotype interactions increased MetS risk, which was further exacerbated by a low plasma polyunsaturated to saturated fat exposure, indicating important modulation of genetic risk by dietary fat exposure.
This was accompanied with predomination of IL-10 over pro-inflammatory cytokines tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), and interleukin-17 (IL-17) in the sera as well as Gal-3 over TNF-α and IL-17 in feces of UC patients with MetS.
In the logistic regression model adjusted for age and sex, higher IL-6 and lower IGF-1 levels confer increased risk of having MetS and its two underlying pathophysiological abnormalities, i.e., visceral obesity and insulin resistance.
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.
Using quantitative real-time PCR, we could show that the expression of intercellular adhesion molecule 1 (ICAM-1), tumor necrosis factor alpha (TNF-alpha), and interleukin 6 (IL-6) significantly increased in peripheral blood leukocytes from "MetS" subjects (n=39) compared to "no MetS" subjects (n=35) 2 h after an oral glucose tolerance test (ICAM-1 +52%, TNF-alpha +107%, and IL-6 +38%) and also in vitro after 72 h cultivation in high-glucose medium (ICAM-1 +74%, TNF-alpha +71%, and IL-6 +44%).
We previously found that blood C-reactive protein (CRP), interleukin-6 (IL-6), and leptin levels were predictors of current metabolic syndrome in schizophrenia.
Patients with MS showed higher levels of interleukin-6 (IL; 2.1 +/- 1.2 vs. 1.2 +/- 0.9 pg/mL, P < 0.05) and reduced FMV (5.4 +/- 3.9 vs. 8.3 +/- 3.1%, P < 0.05).
There was an association between the presence of the rs1800796polymorphism of the IL-6 gene, with BMI (P = 0.031), high-density lipoprotein (HDL) (P = 0.010) and low-density lipoprotein (LDL) (P = 0.037), while this genetic variant did not show any significant association with the presence of MetS as defined by the IDF.
Manipulation of iron status with ferric ammonium citrate and hepcidin-25 induced monocyte chemoattractant protein (MCP)-1 and interleukin-6 in human differentiating monocytes of patients with hyperferritinemia associated with the metabolic syndrome (n=11), but not in subjects with hemochromatosis or HFE mutations impairing iron accumulation (n=15), and the degree of induction correlated with the presence of carotid plaques, detected by echocolor-Doppler.
IL6 serum levels were significantly higher in the MDD group when compared to the healthy control group, and in MDD+MS group when compared to the healthy control group.
Cardiac myocyte injury and stress markers (troponin and natriuretic peptides), markers of renal function (glomeral filtration rate, cystatin-C), and inflammation markers/mediators (interleukin- 6, CRP) are promising biomarkers of patients with AF and MetS.
Before and after the intervention, the components of metabolic syndrome, insulin sensitivity (Matsuda index), and inflammation profile (interleukin-6 and C-reactive protein) were evaluated.
Strong associations with arrhythmia were observed for IL-6 (median 3.90 vs 1.89 pg/mL, p<0.00001) and CRP concentration (6.32 vs 1.47 mg/L, p=0.00009), while MS was associated most strongly with IL-6.
To identify genetic variants in promoter areas of IL-6 -174 G>C and TNF-α -308 G>A in metabolic syndrome (Met S) and controls and associate them with Met S and serum cytokine levels.It was a cross-sectional study, including 224 cases of Met S and 200 controls.