scholarly journals Reduced Expression of Prostacyclin Synthase and Nitric Oxide Synthase in Subcutaneous Arteries of Type 2 Diabetic Patients

2013 ◽  
Vol 231 (3) ◽  
pp. 217-222 ◽  
Author(s):  
Siti Safiah Mokhtar ◽  
Paul M. Vanhoutte ◽  
Susan W.S. Leung ◽  
Mohd Imran Yusof ◽  
Wan Azman Wan Sulaiman ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Oxide Synthase ◽  
Prostacyclin Synthase ◽  
Type 2 Diabetic

Uncoupling of Vascular Endothelial Growth Factor (VEGF) and Inducible Nitric Oxide Synthase (iNOS) in Gingival Tissue of Type 2 Diabetic Patients

Inflammation ◽  
2015 ◽  
Vol 39 (2) ◽  
pp. 632-642 ◽  
Author(s):  
Guendalina Lucarini ◽  
Giacomo Tirabassi ◽  
Antonio Zizzi ◽  
Giancarlo Balercia ◽  
Alexia Quaranta ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Gingival Tissue ◽  
Diabetic Patients ◽  
Vascular Endothelial ◽  
Type 2 Diabetic Patients ◽  
Oxide Synthase ◽  
Endothelial Growth Factor ◽  
Type 2 Diabetic ◽  
Inducible Nitric Oxide

scholarly journals Inflammation and nitric oxide production in skeletal muscle of type 2 diabetic patients

2004 ◽  
Vol 181 (3) ◽  
pp. 419-427 ◽  
Author(s):  
SH Torres ◽  
JB De Sanctis ◽  
L M de Briceno ◽  
N Hernandez ◽  
HJ Finol
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Inflammatory Process ◽  
Tnf Alpha ◽  
Diabetic Patients ◽  
Nitric Oxide Production ◽  
Type 2 Diabetic Patients ◽  
Oxide Synthase ◽  
Type 2 Diabetic

An inflammatory process may be involved in nitric oxide production in skeletal muscle of type 2 diabetic patients. Nitric oxide generation in skeletal muscle was assessed in 14 non-complicated type 2 diabetic patients and in 12 healthy subjects. In samples of quadriceps femoris muscle, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), nitrite, nitrate and nitrotyrosine were determined. The macrophage-specific antigen CD163, the T-cell membrane factor CD154 and tumour necrosis factor-alpha (TNF-alpha) were also assayed. In six patients, ultrastructural analysis of muscle was performed. Nitrites and nitrates were increased in patients as compared to controls (22.7+/-4.5 and 32.7+/-7.0 vs 16.0+/-2.9 and 22.8+/-4.0 micromol/mg protein; P<0.001, Mann-Whitney U test). Endothelial NOS was similar in diabetic and control subjects (36.4+/-13.8 vs 36.3+/-6.8 ng/mg protein), contrasting with the significant increase of iNOS recorded in patients (34.3+/-13.0 vs 8.5+/-2.8 ng/mg protein, P<0.00002). Nitrotyrosine levels were higher in the patient than in the control group (42.1+/-24.4 vs 10.3+/-2.5 ng/mg protein, P<0.00002), as were CD163 (10-fold) and TNF-alpha (fourfold) levels. Furthermore, CD154 levels were detectable only in the patient samples (10.2+/-5.3 ng/mg protein). By multiple-regression analysis, changes in glycated haemoglobin values could predict 96% variation in nitrotyrosine. Macrophages were present in all muscle samples analysed by electromicroscopy. The increased levels of CD163, CD154 and TNF-alpha indicate that an inflammatory process occurs in skeletal muscle of type 2 diabetic patients. This may contribute to iNOS induction, muscle damage and insulin resistance.

The Influence Of Endothelial Nitric Oxide Synthase (Enos) Genetic Polymorphisms On Cholesterol Blood Levels Among Type 2 Diabetic Patients On Atorvastatin Therapy

2020 ◽  
Vol 20 ◽  
Author(s):  
Sarah Abdullah ◽  
Yazun Jarrar ◽  
Hussam Alhawari ◽  
Eyada Abed ◽  
Malek Zihlif
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Lipid Profile ◽  
Genetic Polymorphisms ◽  
Endothelial Nitric Oxide Synthase ◽  
Diabetic Patients ◽  
Enos Gene ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Background: Endothelial nitric oxide synthase (eNOS) plays a major role in the response of antihypercholesterol statin drugs. Genetic polymorphisms in the eNOS gene affect the activity of eNOS and thereby modulate statin response. Objectives: This study investigated the influence of major functional eNOS gene polymorphisms (rs2070744, rs1799983, and rs61722009) on the lipid profile of type 2 diabetes mellitus (T2DM) Jordanian patients treated with atorvastatin. Methods: The sample comprised 103 T2DM patients who attended the diabetes clinic of Jordan University Hospital. The T2DM patients had regularly been taking 20 mg atorvastatin. The atorvastatin response was calculated by measuring the lipid profile before and after three months of atorvastatin treatment. The eNOS genotypes of the subjects were analyzed using polymerase chain reaction (PCR) followed by restriction fragment length polymorphism (RFLP) assay. Results: No significant association was found between eNOS genetic polymorphisms and the response to atorvastatin (ANOVA, p > 0.05). In addition, no significant difference in the frequency of eNOS genotypes was found between T2DM patients and healthy subjects. However, patients with eNOS rs1799983, 4a/4a, and rs61722009 G/G genotypes showed a significantly lower levels of baseline total cholesterol (TC) and low density lipoprotein (LDL) than did patients carrying the rs1799983 4b/4b or rs61722009 T/T genotype (p < 0.05). The eNOS rs1799983 and rs61722009 polymorphisms were in complete linkage disequilibrium (D' = 1). Conclusion: Although no association was found between eNOS genetic polymorphisms and atorvastatin response, there was a significant association between the rs1799983 and rs61722009 genotypes and baselines levels of TC and LDL in Jordanian T2DM patients. These genetic variants affect cholesterol levels and may play a role in the susceptibility to cardiovascular diseases in T2DM patients. Further studies are needed to validate these findings.

scholarly journals Failure of Isoflurane Cardiac Preconditioning in Obese Type 2 Diabetic Mice Involves Aberrant Regulation of MicroRNA-21, Endothelial Nitric-oxide Synthase, and Mitochondrial Complex I

2018 ◽  
Vol 128 (1) ◽  
pp. 117-129 ◽  
Author(s):  
Zhi-Dong Ge ◽  
Yingchuan Li ◽  
Shigang Qiao ◽  
Xiaowen Bai ◽  
David C. Warltier ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Nicotinamide Adenine Dinucleotide ◽  
Endothelial Nitric Oxide Synthase ◽  
Complex I ◽  
Nicotinamide Adenine ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Type 2 Diabetic

Abstract Background Diabetes impairs the cardioprotective effect of volatile anesthetics, yet the mechanisms are still murky. We examined the regulatory effect of isoflurane on microRNA-21, endothelial nitric-oxide synthase, and mitochondrial respiratory complex I in type 2 diabetic mice. Methods Myocardial ischemia/reperfusion injury was produced in obese type 2 diabetic (db/db) and C57BL/6 control mice ex vivo in the presence or absence of isoflurane administered before ischemia. Cardiac microRNA-21 was quantified by real-time quantitative reverse transcriptional–polymerase chain reaction. The dimers and monomers of endothelial nitric-oxide synthase were measured by Western blot analysis. Mitochondrial nicotinamide adenine dinucleotide fluorescence was determined in Langendorff-perfused hearts. Results Body weight and fasting blood glucose were greater in db/db than C57BL/6 mice. Isoflurane decreased left ventricular end-diastolic pressure from 35 ± 8 mmHg in control to 23 ± 9 mmHg (P = 0.019, n = 8 mice/group, mean ± SD) and elevated ±dP/dt 2 h after post-ischemic reperfusion in C57BL/6 mice. These beneficial effects of isoflurane were lost in db/db mice. Isoflurane elevated microRNA-21 and the ratio of endothelial nitric-oxide synthase dimers/monomers and decreased mitochondrial nicotinamide adenine dinucleotide levels 5 min after ischemia in C57BL/6 but not db/db mice. MicroRNA-21 knockout blocked these favorable effects of isoflurane, whereas endothelial nitric-oxide synthase knockout had no effect on the expression of microRNA-21 but blocked the inhibitory effect of isoflurane preconditioning on nicotinamide adenine dinucleotide. Conclusions Failure of isoflurane cardiac preconditioning in obese type 2 diabetic db/db mice is associated with aberrant regulation of microRNA-21, endothelial nitric-oxide synthase, and mitochondrial respiratory complex I.

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