TNF-α: decreased in healthy, fatty liver, IBD and hepatic cirrhosis, no change in diabetes, metabolic syndrome (MS) + PCOS (polycystic ovary syndrome) and arthritis.
No differences were found in the levels of IL-17A, IL-1β, and TNF-α in the diabetes with DE and diabetes without DE groups compared to the normal group (P > .05).
The depletion of MDMs by clodronate liposomes alleviated diabetes-induced tactile allodynia (<i>P</i> < 0.05) and reduced the infiltration of MDMs (<i>P</i> < 0.001) as well as the expression of IL-1<i>β</i> and TNF-<i>α</i> in the spinal cord (<i>P</i> < 0.05).
Vitamin E also significantly (<i>p</i> < .05) inhibited MIA+STZ-induced blood levels of the inflammatory biomarkers, tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) that are known to be modulated in OA and diabetes.
In individuals with diabetes, mtDNA copy number was negatively associated with GSTK1 expression (β = -0.235, P = 0.036) and positively associated with serum high-sensitive C-reactive protein (hsCRP) (β = 0.839, P < 0.001), tumour necrosis factor alpha (TNF-α) (β = 0.549, P < 0.001), interleukin-6 (IL-6) (β = 0.589, P = 0.006) and NEFA (β = 0.001, P = 0.020).
In baseline assessments from the CROSSROADS randomized controlled trial, serum interleukin-6 (IL-6), tumor necrosis factor-α (TNFα) and C-reactive protein (hs-CRP) were assayed in 163 older adults (37% males, 24% African American, BMI 34±3, age 70±5yrs) with hypertension, dyslipidemia and/or diabetes.
In summary, our results indicate widespread methylation differences in DKD kidneys and highlights epigenetic changes in the TNF locus and its contribution to the development of nephropathy in patients with diabetes mellitus.
In separate individual exposure analyses, higher 8-OHdG, hsCRP, and IL-6 (but not TNF) were each independently associated with increased risk of death in multivariate models adjusted for age, sex, diabetes mellitus, cardiovascular disease, protein-energy wasting, cohort calendar year, blood sample storage time and eGFR.
It was shown that DM resulted in severe learning and memory deficits associated with endothelial dysfunction, increased expression of TNF-α and IL-1β, increased oxidative stress levels and decreased expression of eNOS and BDNF.
Rats in the diabetes mellitus group exhibited significantly decreased systolic cardiac function along with elevated expression levels of phosphorylated (p)-PKCβ<sub>2</sub>, phos-P66<sup>shc</sup>, caspase-3, malondialdehyde, collagen type I, tumor necrosis factor-α and interleukin-1β, which were accompanied by disorder in metabolic processes.
The inflammatory process in diabetes is associated with the secretion of inflammatory cytokines by endothelial cells, e.g., tumor necrosis factor alpha (TNFα) and interleukin 6 (IL-6), and with the reduction of cell proliferation.
Serum diagnostic markers of diabetes (insulin, glucose and glycated hemoglobin), inflammatory mediators (tumor necrosis factor-α, interleukin-6, and nitric oxide), and oxidative stress (total antioxidant capacity and reduced glutathione and malondialdehyde) were assayed.
OGA mRNA levels were also increased in leucocytes from patients with diabetes and were correlated with mRNA coding for two pro-inflammatory proteins, TNFα and TxNIP.Therefore, OGA activity in leucocytes might be a more easily accessible biomarker than OGA expression levels.
This study evaluated differences of TPC and TNF-α concentrations in tears at different severity of NPDR among participants with diabetes in comparison with normal participants.
The hazard ratio (HR, 95% confidence interval) for diabetes was significantly reduced in patients receiving TNF inhibitors, HR 0.35 (0.13, 0.91), compared to patients treated with non-biologic DMARDs other than hydroxychloroquine and methotrexate.
The core of protein-protein interaction is the tumor necrosis factor inflammatory pathway, indicating the connection between inflammation and diabetes.
TNF-α levels in STZ-induced DM group were significantly decreased compared to control group (<i>P</i> < 0.05), and groups of DM + HP and DM + Q had higher serum TNF-α levels than STZ-induced DM group (<i>P</i> < 0.05).
A negative association between TNF-α and 25(OH)D was observed (r=-0.197, p=0.003), which was significant only in the subgroup without DM (r=-0.304, p=0.001).
Diabetes decreased glutathione content, and increased reactive oxygen species, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α production in heart and kidney.