The pooled results obtained by using the random-effects model showed that resveratrol supplementation significantly decreased C-reactive protein (CRP) (SMD = -0.55; 95% CI, -0.84, -0.26; P < 0.001; I2: 84.0) and tumor necrosis factor-α (TNF-α) (SMD = -0.68; 95% CI, -1.08, -0.28; P = 0.001; I2: 81.3) concentrations among patients with MetS and related disorders.
This first report on ARL15 expression in RASF and its likely role in inflammation and metabolic syndromes through a TNF independent pathway, encourages hypothesis-free studies to identify additional pathways underlying RA disease biology.
An energy-dense diet, which induces sequelae of the metabolic syndrome in humans and mice at least in part by enhancing pro-inflammatory TNFα formation, has recently been demonstrated to stimulate FGF23 production.
Factors associated with MS were female sex (prevalence ratio [PR]=2.16; 95% CI, 1.04-4.49), age-adjusted institutionalization time >50% (PR=2.38, 95% CI, 1.46-3.88), and high concentrations of interleukin-6 (PR=2.01; 95% CI, 1.21-3.32) and tumor necrosis factor-α (PR=1.70; 95% CI, 1.05-2.77).
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.
Ameliorated TNF-α-induced inflammation and insulin resistance in adipocytes via activation of insulin signaling and enhanced GLUT4 translocation suggesting a reduced hyperglycemia associated with the metabolic syndrome.
They accepted the treatment of NB-UVB and the following data were collected: serum levels of IL-17 (interleukin), TNF-α (tumor necrosis factor) and IL-6, Psoriasis Area and Severity Index (PASI) scores before and after 10 sections of NB-UVB treatment.Significant PASI improvement was observed in psoriatic patients without MS after 10 sections of phototherapy, while patients with MS showed a less improvement (P < .001).
The FF tumor necrosis factor-α (TNF-α) level in the PCOS MS group was 3.89±1.18ng/mL, which was significantly higher compared with the control (2.94±1.02ng/mL) and PCOS non-MS groups (3.05±1.21ng/mL) (P=0.002), while the granulocyte colony-stimulating factor (G-CSF) level in the PCOS MS group (4.18±1.33ng/mL) was lower compared with the control (5.61±1.82ng/mL) and PCOS non-MS groups (5.32±1.91ng/mL) (P=0.004).
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).
Comparing MetS patients to non-MetS IBD patients, there was no significant difference between IBD medication use (i.e., steroids, anti-TNFs, and immunomodulators) or NAFLD medication use, other than statins.
Participants with or without the MetS exhibited contrasting responses to the modified breakfast: respectively, significant changes in DBP levels (-3.7 ± 6.9 versus -0.5 ± 6.9 mm Hg; P < 0.05), plasma glucose (-3 ± 7.3 versus 3 ± 7.4 mg/dL; P < 0.05), and apolipoprotein-B (-0.1 ± 0.6 versus 0.2 ± 0.3 mg/mL; P < 0.05), interferon-γ (-0.6 ± 1.2 versus 0.1 ± 1.3 pg/mL; P < 0.05), and tumor necrosis factor-α concentrations (0.4 ± 3.6 versus -0.8 ± 2.8 pg/mL; P < 0.05) were observed.
Consumption of high-energy-dense foods was associated with increased chance of MetS, most of its features and inflammatory markers including hs-CRP, TNF-α and IL-6.
Increased TNFα in TJA-MetS compared to TJA+MetS may be an artifact of differing sample populations or a true complication of the complex pathophysiology and medical regimen seen in patients with both OA and MetS.
Here, we recruited 248 asthmatic patients, who were separated into asthma with Mets/asthma without Mets groups and 226 matched healthy controls from Hebei Province to evaluate the influence of TNF-α-308G/A polymorphism on metabolic syndrome in asthmatic patients.
This paper aims to investigate the association between psychological stress and MS with respect to the tumor necrosis factor alpha (TNFα) and neuropeptide Y (NPY) genes in the Han and Hui ethnic groups.
These results suggest that the rs1800629 at the tumor necrosis factor alpha gene interacts with MedDiet to influence TG metabolism and inflammation status in MetS subjects.
Moreover, for three of the five components of MetS - waist circumference, fasting plasma triglycerides, systolic blood pressure - an increase was associated with increased GCF TNF-α level in boys.No such findings were seen in girls.
Three genes in EDdb (ADIPO (adiponectin), TNF (tumor necrosis factor) and NR3C1 (nuclear receptor subfamily 3, group C, member 1)) link the KEGG (Kyoto Encyclopedia of Genes and Genomes) "adipocytokine signaling pathway" with the BioCarta "visceral fat deposits and the metabolic syndrome" pathway to form a joint pathway.
The objective of this work was to determine the role of TNFα-308G/A gene polymorphism in metabolic syndrome (MetS) and coronary artery disease (CAD) with obesity and type 2 diabetes mellitus (T2DM).