Serum selenium and glutathione peroxidase concentrations in type 2 diabetes mellitus patients

Kornhauser, Carlos; García-Ramírez, Juana Rosalba; Wróbel, Katarzyna; Pérez-Luque, Elva-Leticia; Garay‐Sevilla, Ma. Eugenia

doi:10.1016/j.pcd.2008.02.003

Cited by 77 publications

(50 citation statements)

References 30 publications

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“…The higher urea level in T2D could be a result of lower urea excretion in attempting to produce more concentrated urine (Bankir et al, 1993). This profile of renal function markers, higher urea, and lower creatinine levels in T2D compared to controls was similar to that found by Kornhauser et al (2008).…”

Section: Discussionsupporting

confidence: 88%

Polymorphism E23K (rs5219) in the KCNJ11 gene in Euro-Brazilian subjects with type 1 and 2 diabetes

et al. 2017

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ABSTRACT. Insulin secretion is regulated by ATP-sensitive potassium channels (KATP). The potassium inwardly-rectifying channel, subfamily J, member 11 (KCNJ11) gene, located on chromosome 11p15.1, encodes the subunit Kir6.2 that forms the pore region of KATP channels in pancreatic β-cells. Among the single nucleotide polymorphisms (SNPs) associated with KCNJ11, the E23K polymorphism (rs5219) promotes a substitution (G > A) of a glutamic acid residue for lysine at position 23. The E23K SNP has been associated with diabetes in several populations, although with controversial results. The aim of this study was to evaluate the association of the E23K SNP with type 1 and 2 diabetes in a case-control study approved by the Ethics Committee. We genotyped 458 Euro-Brazilian individuals, classified as healthy (control group, CTRL, N = 217), patients with type 1 diabetes mellitus (T1D, N = 102), and patients with type 2 diabetes mellitus 2 S.W. Souza et al. Genetics and Molecular Research 16 (2): gmr16029543(T2D, N = 139). Genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) using BanII restriction digestion. The restriction fragments were separated by polyacrylamide gel electrophoresis and visualized by ethidium bromide staining. The genotype (EE/EK/KK) frequencies (%) for the CTRL group (38.2/50.2/11.6), T1D (34.3/52.0/13.7), and T2D (38.2/48.9/12.9) were in Hardy-Weinberg equilibrium and there were no significant differences (CRTL vs T1D, P = 0.771; CRTL vs T2D, P = 0.937; T1D vs T2D, P = 0.831). The minor allele frequencies (MAF; K) for CTRL (37.0%), T1D (39.7%), and T2D (37.4%) were not different among the groups (P > 0.05). The MAF value for healthy subjects was similar to other Caucasian populations (34.5-37.5%). In summary, the E23K polymorphism (rs5219) was not associated with type 1 or 2 diabetes mellitus in the studied population.

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Section: Discussionsupporting

confidence: 88%

Polymorphism E23K (rs5219) in the KCNJ11 gene in Euro-Brazilian subjects with type 1 and 2 diabetes

et al. 2017

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“…22,23 Undoubtedly, any treatment that is able to stabilize oxygen metabolism and modulate oxidative stress would help to delay the onset of DKD in diabetes mellitus. Probucol is a potent lipidsoluble antioxidant with two phenolic hydroxyl group that has been shown to reduce O 2 production, scavenge lipid peroxidation, and inhibit DNA damage, although it is a cholesterol-lowering drug used clinically.…”

Section: Discussionmentioning

confidence: 99%

Epithelial-to-Mesenchymal Transdifferentiation of Renal Tubular Epithelial Cell Mediated by Oxidative Stress and Intervention Effect of Probucol in Diabetic Nephropathy Rats

et al. 2012

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Objective: To elucidate the relationship of oxidative stress and specificity protein 1 (Sp1) in the process of epithelial-tomesenchymal transdifferentiation (EMT) and also to investigate the molecular mechanism of protective effect of probucol on the pathogenesis of diabetic kidney disease (DKD). Methods: Thirty male Sprague-Dawley (SD) rats were randomly divided into control group, diabetic group, and diabetic group under probucol therapy (n ¼ 10 per group). The biochemical indicators including 24-h urinary total protein (24-h UTP) excretion, blood glucose (BG), lipids [triglycerides (TGs), total cholesterol (TC)], serum creatinine (Scr), creatinine clearance rate (Ccr), kidney tissue malondialdehyde (MDA) level, and glutathione peroxidase (GSH-Px) activity were assessed in all groups. The renal pathological changes were evaluated by hematoxylin and eosin (HE) and Masson staining. The protein expression of Sp1, α-smooth muscle actin (α-SMA), and Ecadherin was also measured and analyzed by immunohistochemistry and Western blotting. Results: Compared with the control group, the BG, TC, Scr, 24-h UTP, and MDA level of renal tissue increased significantly and the Ccr reduced in the rats of diabetic group (all p < 0.01). The pathological scores and the expression of Sp1 and α-SMA in renal tissue were upregulated (p < 0.01) and the expression of E-cadherin was down-regulated significantly in the diabetic animals (p < 0.01). In the diabetic animals treated with probucol, the renal injuries were alleviated (p < 0.01). Conclusions: Oxidative stress may play an important role in the EMT process of tubular epithelial cells. Probucol could ameliorate renal disease progression in this model of diabetic nephropathy, which might be due to an antioxidant action, down-regulation of Sp1 protein expression, and inhibition of renal tubular EMT.

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“…Many epidemiological studies demonstrated that serum Se levels were lower in diabetic patients than in healthy individuals. [17][18][19] The atrophy and degeneration of pancreatic islets have also been reported in patients with the Se-deficiency syndrome, Keshan disease.…”

Section: )mentioning

confidence: 92%

Effects of Administering Sodium Selenite, Methylseleninic Acid, and Seleno-L-methionine on Glucose Tolerance in a Streptozotocin/Nicotinamide-Induced Diabetic Mouse Model

Ueno

Shimizu

Okuno

et al. 2014

Biological & Pharmaceutical Bulletin

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The effects of administering the selenocompounds, sodium selenite, methylseleninic acid (MSA), and seleno-L-methionine (SeMet) on glucose tolerance were compared in the nicotinamide (NA) and streptozotocin (STZ)-induced diabetic mouse model. ICR mice were intraperitoneally treated twice with STZ (100 mg/ kg) 15 min after an injection of NA (120 mg/kg) at a 1-d interval. Non-fasting blood glucose levels were then monitored weekly while orally administering the selenocompounds at 158 µg Se/kg body weight with free access to a selenium-deficient diet for 5 weeks. The mean body weights of NA/STZ-induced diabetic mice were partly restored by the administration of selenocompounds, while SeMet led to a higher selenium content and glutathione peroxidase 1 activity in the pancreas. Non-fasting and oral glucose tolerance-tested blood glucose levels, which were elevated by NA/STZ, were significantly suppressed by the administration of SeMet. These results suggest that SeMet may improve glucose tolerance in a NA/STZ-induced mild diabetic mouse model by increasing bioavailability in the pancreas.

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Serum selenium and glutathione peroxidase concentrations in type 2 diabetes mellitus patients

Cited by 77 publications

References 30 publications

Polymorphism E23K (rs5219) in the KCNJ11 gene in Euro-Brazilian subjects with type 1 and 2 diabetes

Polymorphism E23K (rs5219) in the KCNJ11 gene in Euro-Brazilian subjects with type 1 and 2 diabetes

Epithelial-to-Mesenchymal Transdifferentiation of Renal Tubular Epithelial Cell Mediated by Oxidative Stress and Intervention Effect of Probucol in Diabetic Nephropathy Rats

Effects of Administering Sodium Selenite, Methylseleninic Acid, and Seleno-L-methionine on Glucose Tolerance in a Streptozotocin/Nicotinamide-Induced Diabetic Mouse Model

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