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.
Duration of DM, fasting plasma glucose (FPG), glycosylated hemoglobin A1c (HbA1c) and also levels of inflammatory cytokines (hs-CRP, TNF-α and IL-6) in the combination with hypertension group were all significantly higher than those in the non-combination with hypertension group (P<0.05).
Analysis of the -308 TNFalpha polymorphism in patients with type 2 diabetes and in control subjects revealed that the heterozygous TNF1/TNF2 genotype was significantly less frequent in the patient group (p=0.003), suggesting that TNF1/TNF2 may be considered as a protective marker against type 2 diabetes (OR=0.58).
The aim of this study was to evaluate the effects of butyrolactone-I (A6) on type 2 diabetes (T2D) in db/db mice because A6 was found to inhibit α-glucosidase activities and TNF-α release, which were associated with improving T2D.
In addition, PPD and PPT dramatically ameliorated the inflammatory responses by suppressing the secretion of pro-inflammatory cytokines like tumor necrosis factor-alpha and interleukin-6 in serum level and gene expression in liver level, and improved the antioxidant capacity by increasing the superoxide dismutase and decreasing malondialdehyde levels in the serum of T2DM mice.
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).
Upregulated expression of resistin, vaspin, apelin and TNF-α plays a significant role in induction of insulin resistance linked with obesity and type 2 diabetes.
Circulating concentrations of acylated ghrelin and TNF-α were increased, whereas desacyl ghrelin levels were decreased in obesity-associated type 2 diabetes.
To explore the links between tumor necrosis factor alpha (TNFalpha) and leptin adipose tissue expression and low-grade systemic inflammation and to determine the relationship between inflammation and the degree of adiposity, the presence of type 2 diabetes, and other cardiovascular risk factors.
The evolutive advantages of increased inflammatory responses, hypersecretion of proinflammatory cytokines [tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, IL-6, and IL-18], or decreased anti-inflammatory molecules (adiponectin, certain TNF-alpha isoforms, soluble CD14, etc.), would lead in westernized countries to chronic inflammation conditions, such as obesity and type 2 diabetes, resulting in cardiovascular disease.
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.
Therefore, this work was planned to evaluate the association of -863C/A (rs1800630) and -1031T/C (rs1799964) polymorphisms in TNF gene with plasma TNF-α levels and DN among subjects with type 2 diabetes (T2DM) in a population from North India.
In addition, ADSC infusion promoted anti-inflammatory cytokine interleukin (IL)-10 expression and inhibited pro-inflammatory cytokines IL-6, IL-1β, and tumor necrosis factor (TNF)-α expression in both the spleen and serum of T2D rats without SPX.
Tumour necrosis factor (TNF)-alpha, which is considered to play a role in obesity-induced non-insulin-dependent diabetes mellitus and to augment oxidative stress, also suppressed PPAR gamma expression.5.
The tumor necrosis factor system plays an important role in the pathogenesis of obesity and type 2 diabetes (DM), by a complex and only partially understood mechanism.