Increased levels of tumour necrosis factor-α (TNF-α) in patients with Type II diabetes mellitus after myocardial infarction are related to endothelial dysfunction

2006 ◽  
Vol 110 (6) ◽  
pp. 673-681 ◽  
Author(s):  
Thomas Nyström ◽  
Arne Nygren ◽  
Åke Sjöholm
Keyword(s):  
Endothelial Dysfunction ◽  
Brachial Artery ◽  
Type Ii Diabetes ◽  
Type Ii Diabetes Mellitus ◽  
Type Ii ◽  
Tumour Necrosis Factor Α ◽  
Brachial Artery Diameter ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

The pathophysiology of insulin resistance and atherosclerosis may share a common inflammatory basis, maintaining endothelial dysfunction, suggesting why patients with T2DM (Type II diabetes mellitus) have an impaired prognosis after an MI (myocardial infarction), but it remains unclear how these parameters are inter-related. Forty patients with an MI (20 patients with and 20 patients without T2DM) took part in this cross-sectional study. Endothelium-dependent [FMD (flow-mediated dilation)] and -independent [NTG (nitroglycerine)] vasodilatation (determined by ultrasound), SI (insulin sensitivity index; determined by isoglycaemic–hyperinsulinaemic clamp) and serum levels of CRP (C-reactive protein), TNF-α (tumour necrosis factor-α), IL-6 (interleukin 6), resistin and adiponectin (determined by ELISA) were measured. Associations between FMD/NTG and SI, and CRP, TNF-α, IL-6, adiponectin, resistin, lipids, blood pressure, BMI (body mass index) and brachial artery diameter were then assessed. FMD (2.1 compared with 4.7%; P<0.05), NTG (14.9 compared with 21.2%; P<0.05) and SI [4.3 compared with 6.6 10−4 dl·kg−1 of body weight·min−1·(μ-units/ml)−1; P<0.05], and adiponectin levels (3.1 compared with 6.4 μg/ml; P<0.01) were all lower in patients with T2DM. TNF-α (6.9 compared with 1.8 pg/ml; P<0.01) and IL-6 (2.3 compared with 1.2 pg/ml; P<0.01) levels were higher in patients with T2DM, whereas differences in CRP and resistin levels did not attain statistical significance between the two groups. TNF-α concentrations and brachial artery diameter were negatively, whereas SI was positively, correlated with FMD. Adjustment for age weakened the association for SI, whereas TNF-α and brachial artery diameter remained significantly associated with FMD after adjustment for group, age and BMI. Endothelial dysfunction and low-grade inflammation co-exist in T2DM after MI. These results suggest that the endothelium is negatively impacted in multiple ways by the diabetic state after an MI.

Effect of lowering tumour necrosis factor-α on vascular endothelial function in Type II diabetes

2002 ◽  
Vol 103 (2) ◽  
pp. 163-169 ◽  
Author(s):  
William BILSBOROUGH ◽  
Gerard O'DRISCOLL ◽  
Kim STANTON ◽  
Rukshen WEERASOORIYA ◽  
Lawrence DEMBO ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Tumour Necrosis Factor ◽  
Brachial Artery ◽  
Type Ii Diabetes ◽  
Tumour Necrosis ◽  
Type Ii ◽  
Tumour Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

Tumour necrosis factor-α (TNFα) is a mediator of reactive oxygen species, which are implicated in endothelial dysfunction and atherosclerosis. Type II diabetes is associated with endothelial dysfunction and elevated circulating TNFα. We hypothesized that reducing serum levels of TNFα, using pentoxifylline, would improve endothelial function. Thirteen subjects [age 58±2 (S.E.M.) years] with Type II diabetes (disease duration 74±13months) undertook a randomized, crossover study of 8weeks pentoxifylline and 8weeks placebo. Endothelium-dependent and-independent vasodilation in resistance arteries was assessed via bilateral forearm venous occlusion plethysmography during intra-brachial infusions of acetylcholine (ACh), sodium nitroprusside (SNP) and NG-monomethyl-l-arginine (l-NMMA). High-resolution ultrasound of the brachial artery in response to ischaemia was used to determine endothelium-dependent conduit vessel flow-mediated dilation (FMD), and endothelium-independent conduit function was assessed by sublingual administration of glyceryl trinitrate (GTN). Serum concentrations of TNFα were also determined. Pentoxifylline lowered serum TNFα from 4.1±0.7 to 2.9±0.6 pg˙ml-1 (P = 0.001). Forearm blood flow (FBF) responses at each dose of ACh did not differ with treatment (P = 0.4). Similarly, FBF responses to SNP (P = 0.8) and l-NMMA (P = 0.2) did not differ. There was also no significant difference in brachial artery diameter during FMD (P = 0.2) or GTN administration (P = 0.06). Despite lowering serum TNFα concentration, pentoxifylline at a dose of 400mg three times a day for 8weeks did not improve vascular function in either conduit or resistance vessels in this group of Type II diabetic subjects.

scholarly journals Coenzyme Q10 improves endothelial dysfunction of the brachial artery in Type II diabetes mellitus

Diabetologia ◽  
2002 ◽  
Vol 45 (3) ◽  
pp. 420-426 ◽  
Author(s):  
G. F. Watts ◽  
D. A. Playford ◽  
K. D. Croft ◽  
N. C. Ward ◽  
T. A. Mori ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Endothelial Dysfunction ◽  
Brachial Artery ◽  
Coenzyme Q10 ◽  
Type Ii Diabetes ◽  
Type Ii Diabetes Mellitus ◽  
Type Ii

Effect of lowering tumour necrosis factor-α on vascular endothelial function in Type II diabetes

2002 ◽  
Vol 103 (2) ◽  
pp. 163 ◽  
Author(s):  
William BILSBOROUGH ◽  
Gerard O’DRISCOLL ◽  
Kim STANTON ◽  
Rukshen WEERASOORIYA ◽  
Lawrence DEMBO ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Tumour Necrosis Factor ◽  
Type Ii Diabetes ◽  
Tumour Necrosis ◽  
Vascular Endothelial ◽  
Type Ii ◽  
Tumour Necrosis Factor Α ◽  
Vascular Endothelial Function ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Estimation of Plasma Levels of Tumor Necrosis Factor-α, Interleukin-4 and 6 in Patients with Chronic Periodontitis and Type II Diabetes Mellitus

2018 ◽  
Vol 19 (2) ◽  
pp. 166-169 ◽  
Author(s):  
Jasjit Sahota ◽  
Dipanshu Bakshi ◽  
Guneet Kaur ◽  
Deepinder Singh ◽  
Ambika Thakur ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Tumor Necrosis Factor ◽  
Chronic Periodontitis ◽  
Type Ii Diabetes ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Type Ii Diabetes Mellitus ◽  
Type Ii ◽  
Tnf Α ◽  
Factor Α

ABSTRACT Introduction Both periodontitis and type II diabetes mellitus (T2DM) are common diseases with a multifactorial etiology and have influence of cytokines in their pathogenesis and thus may also influence each other. In recent times, more attention has been given to understanding the influences of these inflammatory cytokines which are a main part of oral chronic inflammation on systemic health of the individuals. Therefore, the aim of this study was to evaluate the plasma cytokine levels, specifically tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-4, in chronic periodontitis patients and T2DM patients, so as to investigate the influence of chronic periodontitis in systemic inflammation associated with diabetes mellitus. Materials and methods The present study comprised a total sample size of 60 patients. A detailed history along with complete periodontal examination were done for each person. These patients were subdivided into four study groups with 15 subjects (n = 15) in each group: group I: healthy individuals, group II: chronic periodontitis, group III: diabetes mellitus without chronic periodontitis, and group IV: diabetes mellitus with chronic periodontitis. Venous blood was withdrawn for obtaining serum samples from the subjects. Hemoglobin A1c (HbA1c) levels were measured from the automated chromatography. Using enzyme-linked immunosorbent assay kit, TNF-α, IL-4, and IL-6 were measured. Results It was observed that the difference between almost all the results showed statistical significance. Not much of a difference was seen when TNF-α and IL-6 findings of group II were compared with group III. Furthermore, IL-4 also did not differ when group II was compared with group IV. Conclusion The inflammatory cytokines together control the inflammation process and a balance is maintained. However, in patients with diabetes mellitus, this balance is interrupted, which affects the final development and progression of the disease. Thus, hyperglycemia may be partly associated with the severity of the periodontal status in diabetic patients. Clinical significance Hyperglycemia thus may play a role in increasing the severity of the periodontal status in diabetic patients. Keeping such relationship in mind, better treatment modalities can be provided to the patients. How to cite this article Bakshi D, Kaur G, Singh D, Sahota J, Thakur A, Grover S. Estimation of Plasma Levels of Tumor Necrosis Factor-α, Interleukin-4 and 6 in Patients with Chronic Periodontitis and Type II Diabetes Mellitus. J Contemp Dent Pract 2018;19(2):166-169.

Determinants of brachial artery mean 24 h pulse pressure in individuals with Type II diabetes mellitus and untreated mild hypertension

2002 ◽  
Vol 102 (2) ◽  
pp. 177 ◽  
Author(s):  
Robert A. J. M. van DIJK ◽  
Frans J. van ITTERSUM ◽  
Nico WESTERHOF ◽  
Els M. van DONGEN ◽  
Otto KAMP ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Brachial Artery ◽  
Pulse Pressure ◽  
Type Ii Diabetes ◽  
Mild Hypertension ◽  
Type Ii Diabetes Mellitus ◽  
Type Ii

Differential effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α, interleukin-6 and corticosterone induced by bacterial lipopolysaccharide in mice

1995 ◽  
Vol 144 (3) ◽  
pp. 457-462 ◽  
Author(s):  
G Haskó ◽  
I J Elenkov ◽  
V Kvetan ◽  
E S Vizi
Keyword(s):  
Tumour Necrosis Factor ◽  
Interleukin 6 ◽  
Plasma Levels ◽  
Tumour Necrosis ◽  
Endotoxin Shock ◽  
Bacterial Lipopolysaccharide ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Abstract The effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and corticosterone induced by bacterial lipopolysaccharide (LPS) was investigated in mice using ELISA and RIA. It was found that the LPS-induced TNF-α response was significantly blunted in mice pretreated with CH-38083, a novel and highly selective α2-adrenoreceptor antagonist (the α2/α1 ratio is >2000). In contrast, LPS-induced increases in both corticosterone and IL-6 plasma levels were further increased by CH-38083. Since it has recently been shown that the selective block of α2-adrenoreceptors located on noradrenergic axon terminals resulted in an increase in the release of noradrenaline (NA), both in the central and peripheral nervous systems, and, in our experiments, that propranolol prevented the effect of α2-adrenoreceptor blockade on TNF-α plasma levels induced by LPS, it seems likely that the excessive stimulation by NA of β-adrenoreceptors located on cytokine-secreting immune cells is responsible for this action. Since it is generally accepted that increased production of TNF-α is involved in the pathogenesis of inflammation and endotoxin shock on the one hand, and corticosterone and even IL-6 are known to possess anti-inflammatory properties on the other hand, it is suggested that the selective block of α2-adrenoreceptors might be beneficial in the treatment of inflammation and/or endotoxin shock. Journal of Endocrinology (1995) 144, 457–462

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