TNF-α: decreased in healthy, fatty liver, IBD and hepatic cirrhosis, no change in diabetes, metabolic syndrome (MS) + PCOS (polycystic ovary syndrome) and arthritis.
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.
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).
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.
The core of protein-protein interaction is the tumor necrosis factor inflammatory pathway, indicating the connection between inflammation and diabetes.
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.
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.
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.
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).
The association of non-alcoholic fatty liver disease (NAFLD) with insulin resistance (IR) is well established, yet little is known of their possible relationship with intrahepatic iron and serum tumour necrosis factor (TNF)-α concentrations in adults without diabetes.
We hypothesized that circulating osteoprotegerin (OPG) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) levels could be associated with vascular calcification, which is predominant in diabetes.The study included 71 Korean participants (36 with diabetes and 35 without diabetes), who were sub-grouped according to the results of the ankle-brachial index (ABI) and/or X-ray computed tomography scan (CT scan).
Diabetes decreased glutathione content, and increased reactive oxygen species, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α production in heart and kidney.
In mouse models of obesity and diabetes, JTP-96193 reduced the TNF-α release from the fat tissue and prevented development of diabetes and improved insulin resistance, respectively.
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.
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.
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.
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).
In this study, it was aimed to investigate the effects of <i>hesperidin</i> (HP) and <i>quercetin</i>, which are natural flavonoids, on serum malondialdehyde (MDA), glutathione (GSH), tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6) levels in rats with streptozotocin (STZ)-induced diabetes.
In general, concentric and isometric torques were lower and tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β plasma levels were higher in the groups with diabetes than in controls.