Diabetes increased malondialdehyde (MDA) concentration by 39%; elevated levels of TNF-α (44%) and IFN-γ (20%); and reduced the antioxidant status in the kidney in comparison to normal control rats.
Diabetes decreased glutathione content, and increased reactive oxygen species, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α production in heart and kidney.
Tumour necrosis factor alpha (TNF) mRNA expression has been reported to be up-regulated in adipose tissue from several rodent models of obesity and diabetes and from obese humans.
Tumor necrosis factor-alpha-induced inflammatory gene expression, H3K4me2 levels, and recruitment of RNA polymerase II at the gene promoters were also enhanced in db/db VSMCs, demonstrating the formation of open chromatin poised for transcriptional activation in diabetes.
TNF-α: decreased in healthy, fatty liver, IBD and hepatic cirrhosis, no change in diabetes, metabolic syndrome (MS) + PCOS (polycystic ovary syndrome) and arthritis.
Adjusted for TNF-alpha and IL-1beta polymorphisms, patients with a IL-6 (-174)CC genotype have a 3.0-fold (95% CI: 1.2-7.1) increased risk of developing diabetes before the age of 6 years than (-174)G allele carrier patients.
After adjusting for BMI and other lifestyle factors, all three biomarkers significantly predicted diabetes risk; the odds ratios (ORs) comparing extreme quintiles were 1.64 (95% CI 1.10-2.45) for TNF-alphaR2, 1.91 (1.27-2.86) for IL-6, and 4.36 (2.80-6.80) for CRP (P for trend <0.001 for all biomarkers).
After adjustment in the multivariate regression analysis, the following variables remained significantly associated with HCC-HCV occurrence: diabetes (p=0.012 OR 10.44 CI 1.66-65.60), IL-10 lower levels (p<0.0001 OR 0.83 CI 0.78-0.89) and TNF-α higher levels (p<0.0001 OR 1.19 CI 1.11-1.28).
After administration of BCA, retina concentrations of vascular endothelial growth factor, tumor necrosis factor-alpha and interleukin-1beta decreased in the 2 groups of treated rats with diabetes compared to the control group with diabetes (p<0.05).
After stratification according to risk factors for CAD, our analysis revealed that CAD patients with diabetes (p=0.042) and CAD patients without hypertension (p= 0.0495) displayed a higher frequency of the TNF -308 AA genotype compared with healthy controls.
Body mass index (BMI), blood pressure variability parameters including baroreflex sensitivity (BRS), spectral indices of heart rate variability, autonomic function tests, insulin resistance, lipid profile, inflammatory markers (interleukin 6, high-sensitivity C-reactive protein, tumor necrosis factor α) and oxidative stress (OS) marker were measured and analyzed in control group (without family history of diabetes; 65 women, 60 men) and study group (FDRs of type 2 diabetics; 52 women, 49 men) subjects.
By contrast, CXCR4 and TNF-<i>α</i> in the spinal cord dorsal horn did not significantly increase at 2 weeks of diabetes while both were significantly upregulated at 5 weeks of diabetes.