Our findings suggest that the GG genotype of TNF-alphaG-308A polymorphism or a genetic variant in close linkage disequilibrium may interact with obesity to increase the risk of nephropathy in Chinese Type 2 diabetic patients.
CONCLUSIONS The rs4918 minor variant is associated with lower TNFα and adiponectin, higher leptin levels in healthy persons, and more favorable anthropomorphic parameters of obesity in cohort 2.
The results of this study suggest that the G allele of G-238A in TNF-α gene may be a risk factor for overweight/obesity in the Korean population and that the C allele of C-857T may be an protective factor in relation to the HDL level in the general Korean population.
The frequency of '-308A'allele in TNFalpha gene was significantly higher in obese subjects with OSA (28.8%; 60/208), when compared with obese subjects without OSA (12.6%; 26/206, p=0.001).
Polymorphisms in the adipokine genes, LEP, LEPR, and RETN were not associated with obesity susceptibility, whereas ADIPOQ G276T (T vs. G: odds ratio (OR), 1.59; 95% confidence interval (CI), 1.39-1.81), IL-1β C3953T (CC vs. CT+TT: OR, 1.61; 95% CI, 1.18-2.20), and TNF-αG308A (GG vs. GA+AA: OR, 1.19; 95% CI, 1.02-1.39) polymorphisms were associated with an increased risk of obesity.
Therefore, the present study illustrates the relationship between TNF-α polymorphism, the degree of inflammation assessed by serum high sensitivity C-reactive protein concentration (CRP-hs) and basal DNA damage in patients with obesity (BMI 30-34.9 kg/m<sup>2</sup>) and control subjects with proper body mass (BMI < 25 kg/m<sup>2</sup>).
The objective of this work was to determine the role of TNFα-308G/A gene polymorphism in metabolic syndrome (MetS) and coronary artery disease (CAD) with obesity and type 2 diabetes mellitus (T2DM).
To investigate whether the G-308A polymorphism of the TNF-α gene may influence obesity, insulin resistance, fasting plasma lipids, serum leptin levels, and the incidence of metabolic syndrome.
For most of the investigated genes (PPARA, PPARG2, UCP1, UCP2, UCP3, BAR-2, APM1, leptin, SORBS1, HSL, and TNFA) an indication for a minor effect on obesity risk was found.
The -675 4G/5G PAI-1 and the -308 TNF-α polymorphism variants tested in this study, individually or combined, were not associated with obesity in an Argentinean population.
Our aim was to compare lipid, glucose-insulin and inflammatory (tumor necrosis factor alpha; TNF-α) profiles, muscle function, energy expenditure and aerobic capacity between healthy normal-weight (NW) adults, metabolically healthy obese (MHO) and metabolically unhealthy obese (MUHO) adults; to study the associations between these outcomes and the cytokines MSTN, ADP, LP; and to establish cutoffs for MSTN and LP/ADP to identify the MUHO phenotype.
Thus, a decreased processing rate of mTNF-alpha in mature adipocytes combined with an increase in TNF-alpha production may be a potential mechanism resulting in elevated membrane-associated TNF-alpha in adipose tissue in obesity.
We analysed the levels of cytokines (tumour necrosis factor [TNF] α and interleukins [ILs] 1β, 4, 6 and 10), chemokines (stromal cell derived factor 1α, monocyte chemoattract protein [MCP] 1, eotaxin and fractalkine) and growth factors (brain-derived neurotrophic factor, pro-fibrotic platelet-derived growth factor [PDGF-BB] and insulin-like growth factor 1) in serum of prepubertal children with obesity (61 girls/59 boys, 50% IR and 50% non-IR) and 32 controls.
We evaluated the association between ghrelin isoforms (acylated and desacyl ghrelin) and TNF-α in obesity and obesity-associated type 2 diabetes, as well as the potential role of ghrelin in the control of apoptosis and autophagy in human adipocytes.
Accordingly, TNF α has been implicated in a wide range of autoimmune and infectious diseases, but also in conditions such as obesity and insulin resistance.
Obesity is associated with the changes of plasminogen activator inhibitor-1 (PAI-1), tumor necrosis factor-alpha (TNFalpha) and transforming growth factor beta (TGFbeta) levels.