In conclusion, besides consideration of CRP levels alone, our findings suggested that IL-6 outstandingly plays a contributing role in T2DM progression and elevated TNF-<i>α</i> levels over time could be a potential predictor of T2DM.
In double combination, IL-6 -597 GA and TNF-α -308 GG genotypes increased the risk up to 21 times and in triple combination IL-6 -597 AA, TNF-α -308 GG and IL-10 -592 CA increased the risk of T2DM up to 314 times.
In fact, we evaluated the effect of seven polymorphisms in the following genes-PPARg (Pro12Ala), TNFα (-308A/G), ENPP1(K121Q), TCF7L2(rs7903146°C/T), MTHFR(C677T), ACE(I/D), and CAPN10(3R/2R)-on T2D risk, through a meta-analysis combining data of previous studies performed on Tunisian populations originating from the north, center, or south of the country.
In multivariate logistic regression analysis, MDA,CRP, Hb1c, TNF-a, and FBG were the most predictive risk factors for dementia Conclusions: These results suggest that a decrease in anti-oxidant levels and an increase in anti-inflammatory and oxidative stress markers might be involved in the pathophysiology of cognitive disorder associated with T2DM.
In terms of the molecular mechanisms involved, trigonelline induced the protein expression of peroxisome proliferator-activated receptor (PPAR)-γ and suppressed glucose transporter 4 but suppressed the protein expression of tumor necrosis factor-α and leptin in T2DM rats.
In the present study, we examined the promotion to proinflammatory cytokines and chemokines in type 2 diabetes mellitus (T2DM) patients with bone fractures, and then evaluated the promotion to TNF-α by the high glucose treatment in human osteoblast-like MG-63 cells and the regulatory role of the promoted TNF-α on the MG-63 cell apoptosis.
In the present study, we investigated the associations between anemia and polymorphisms in EPO promoter (rs1617640), TNF-αG-308A and ACE Insertion/Deletion in Chinese patients with type 2 diabetes.
In this direction, we aimed to investigate the relationship among TLR4 and IRAK1, TIRAP gene variants, and type 2 diabetes and insulin resistance, and investigate how these variants affect inflammatory factors (TNF-α, IL-6, MCP-1, and IL-1β).
Increased plasma concentrations of tumor necrosis factor alpha (TNFalpha) system components appear in type 2 diabetes patients with poor glycemic control.
Increased serum levels of TNF-α was not associated with increased risk of painful DPN in patients with type 2 diabetes (OR = 2.486, 95 % CI 0.672-9.193, P = 0.172).
Interestingly, expression of collagen type I, integrin beta-I binding protein-I, pyruvate dehydrogenase kinase, TNF receptor genes up-regulated with DM; on the other hand, IL-33, cholecystokinin, plasminogen activator, IL-1 and serine peptidase inhibitor genes down-regulated significantly.
Interleukin-6 and tumor necrosis factor-alpha are not increased in patients with Type 2 diabetes: evidence that plasma interleukin-6 is related to fat mass and not insulin responsiveness.
It can be concluded that the genetic variant of TNF-α along with elevated TNF-α and FFA concentrations play a role in the development of dyslipidemia which could be a potent risk factor towards T2D in Gujarat population.
l-Carnosine supplementation attenuated fasting glucose, triglycerides, advanced glycation end products, and tumor necrosis factor-α levels in patients with type 2 diabetes: a double-blind placebo-controlled randomized clinical trial.
Levels of immunoglobulin A1 and messenger RNA for interferon gamma and tumor necrosis factor alpha in total saliva from patients with diabetes mellitus type 2 with chronic periodontal disease.
Low-grade arterial inflammation is common to both conditions, and increased levels of tumor necrosis factor-alpha (TNF-alpha) have been reported in both DM and CKD.