Elevated blood viscosity decreases the perfusion of skeletal muscle, leading to myocyte expression of the myokine IL-6, decreased glucose uptake, insulin resistance, hyperglycemia, and metabolic syndrome.
Total ROS, inflammatory parameters and adhesion molecules were enhanced in the presence of MetS (p<0.05), and the PCOS+MetS group showed higher levels of IL-6 and ICAM-1 than controls (p<0.05).
Urinary d<sub>6</sub>-α-CEHC 24-h concentrations were associated with the plasma AUC<sub>0-24 h</sub> of d<sub>6</sub>-α-T (<i>r</i> = 0.53, <i>P</i> = 0.02) and d<sub>6</sub>-α-CEHC (<i>r</i> = 0.72, <i>P</i> = 0.0003), and with urinary d<sub>6</sub>-α-CMBHC (<i>r</i> = 0.88, <i>P</i> < 0.0001), and inversely with the plasma inflammation biomarkers C-reactive protein (<i>r</i> = -0.70, <i>P</i> = 0.0006), interleukin-10 (<i>r</i> = -0.59, <i>P</i> = 0.007), and interleukin-6 (<i>r</i> = -0.54, <i>P</i> = 0.01).<b>Conclusion:</b> Urinary α-CEHC and α-CMBHC are useful biomarkers to noninvasively assess α-tocopherol adequacy, especially in populations with MetS-associated hepatic dysfunction that likely impairs α-tocopherol trafficking.
Anthropometric measures were correlated with the components of MetS (triglycerides, glucose, blood pressure, and high-density lipoprotein cholesterol) as well as inflammation markers (interleukin-6 and tumor necrosis factor-alpha , C-reactive protein, and ceruloplasmin).
Psoriatic patients with MS showed a much less reduction of IL-17 and IL-6 before and after 10 sections of NB-UVB treatment respectively than patients without MS (P < .05).Psoriatic patients with MS have poorer improvement in comparison those without MS using NB-UVB treatment.
IL-6 remains an independent predictive biomarker for LVDD in MetS patients, underlining the importance of IF in the evolution of MetS to subclinical cardiac damage.
The significantly higher distribution of risk polymorphisms in PSEN1 and APOE-ε4 is characteristic of a representative number of patients with Alzheimer's disease; whereas polymorphisms in ACE, AGT(235), and IL6(573), are most probably related with the high number of patients with metabolic syndrome or cerebrovascular damage.
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.
The C allele at the -174 locus of IL-6 gene is independently associated with the occurrence of metabolic syndrome, emphasizing the importance of inflammatory genetic background in the pathogenesis of visceral obesity and related cardiovascular burden.
All PPAR SNPs were not associated with obesity and Met-S in the suburban population of Kampar, Malaysia, where only PPARα V162 and PPARγ2 T161 alleles were associated with plasma IL-6 and HOMA-IR, respectively.
Low COX4I1 was associated with type 2 diabetes in obese patients, adjusting for age, gender, smoking, interleukin-6 and high-sensitivity C-reactive protein, all related to metabolic syndrome (MetS; odds ratio: 6.1, 95% confidence interval: 2.3-16).
The aim of the study was to estimate the influence of interactions between peroxisome proliferator-activated receptor γ (PPARγ) and target genes lipoprotein lipase (LPL), interleukin 6 (IL6), angiotensin converting enzyme (ACE), and angiotensin II type 1 receptor (AT1R) on metabolic syndrome (MetSy) and its traits.
The Overwt-MetSyn group demonstrated a significant elevation in expression of TLR2, TLR4, tumour necrosis factor-a (TNF a) and interleukin-6 (IL6) in peripheral monocytes, and increased circulating levels of TNF a and IL6 when compared with the Overwt-Healthy group.
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.
The minor allele of rs9939609 (FTO), rs7903146 (TCF7L2), C56G (APOA5), T1131C (APOA5), C482T (APOC3), C455T (APOC3) and 174G>C (IL6) were more prevalent in subjects with MetS, whereas the minor allele of Taq-1B (CETP) was less prevalent in subjects with the MetS.
Single-nucleotide polymorphisms in the genes encoding for IL-6 (g.-634G>C; c.174G>C), TNFα (g.-308G>A), methylenetetrahydrofolate reductase (MTHFR) (c.677C>T), APOC3 (c.3175C>G), and APOA5 (g.-1131T>C) have been implicated in the processes of inflammation and energy intake that take place in the development of MetS manifestations.
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.
Finally, patients suffering from the metabolic syndrome with high levels of sCD40L also displayed high levels of IL-6, in line with the concept that CD40L may induce the expression of inflammatory cytokines in vivo in this population.