TNF-α: decreased in healthy, fatty liver, IBD and hepatic cirrhosis, no change in diabetes, metabolic syndrome (MS) + PCOS (polycystic ovary syndrome) and arthritis.
TNF-<i>α</i> inhibition may be a potential strategy for the prevention of metabolic syndrome and could play a role in the reduction of cardiovascular risk in RA.
A prospective study on the prevalence of metabolic syndrome among healthy french families: two cardiovascular risk factors (HDL cholesterol and tumor necrosis factor-alpha) are revealed in the offspring of parents with metabolic syndrome.
A statistically significant decrease in the concentration of TNF-α after treatment was also found (baseline, 5.3 ± 1.4 vs. post-treatment, 3.5 ± 1.3, <i>p</i> < 0.05).Our findings suggest that the consumption of the dry fruit of <i>Sechium edule</i> has an antioxidant and anti-inflammatory effect in older adults with metabolic syndrome.
Additive effect of polymorphisms in the IL-6, LTA, and TNF-{alpha} genes and plasma fatty acid level modulate risk for the metabolic syndrome and its components.
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.
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.
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.
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.
Even Short-Term Telmisartan Treatment Ameliorated Insulin Resistance But Had No Influence on Serum Adiponectin and Tumor Necrosis Factor-Alpha Levels in Hypertensive Patients with Metabolic Syndrome.
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).
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.
In African Americans and whites, neither the TNF2 allele nor another polymorphism in the TNF-alpha gene or a neighboring gene with which the TNF2 allele is in linkage disequilibrium is associated with differences in the level of or increased clustering of components of the insulin resistance syndrome.
In all youth, MetS severity was significantly associated with body fat %, ADP, interleukin-6 (IL-6) and TNF-α and also with CRP in PWS, but associations became non-significant for CRP and IL-6 when controlling for body fat %.
In patients with rheumatoid arthritis (RA), insulin resistance (IR), a component of the metabolic syndrome, is closely linked to the systemic inflammation induced by proinflammatory cytokines such as tumor necrosis factor-α and interleukin (IL)-6.
In this study, we used the galectin 2 (LGALS2) genotype, which affects LTA secretion but is located on another chromosome than the HLA gene cluster or TNF, to examine the relationship between the LTA pathway and traits of the metabolic syndrome.