Reduction of postchallenge hyperglycaemia prevents acute endothelial dysfunction in subjects with impaired glucose tolerance

Wascher, Thomas C.; Schmoelzer, I.; Wiegratz, A.; Stuehlinger, Markus; Mueller-Wieland, Dirk; Kotzka, Jörg; Enderle, M. D.

doi:10.1111/j.1365-2362.2005.01550.x

Cited by 76 publications

(55 citation statements)

References 52 publications

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“…Therefore, the improvement in CAVI observed in our study may be consistent mainly with the improvement of endothelial dysfunction but not the regression of a organic lesion. Endothelial function is known to be affected by many factors, especially by dietary conditions 34,35) ; therefore, further studies to clarify the effects of these factors are required in the future.…”

Section: Discussionmentioning

confidence: 99%

Effects of Pitavastatin, a 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibitor, on Cardio-Ankle Vascular Index in Type 2 Diabetic Patients

Miyashita

Endo

Saiki

et al. 2009

J Atheroscler Thromb

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Aim: A novel device has been developed for measuring the cardio-ankle vascular index (CAVI) as an indicator of arterial stiffness. In this study, we evaluated the effect of pitavastatin on CAVI in type 2 diabetic patients. Methods: Forty-five type 2 diabetes mellitus patients with low-density lipoprotein cholesterolemia were enrolled and treated with pitavastatin 2 mg/day for 12 months. Before and after pitavastatin administration, HbA1c, serum lipids, serum malondialdehyde-LDL (MDA-LDL), urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) and CAVI were measured.

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Section: Discussionmentioning

confidence: 99%

Effects of Pitavastatin, a 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibitor, on Cardio-Ankle Vascular Index in Type 2 Diabetic Patients

Miyashita

Endo

Saiki

et al. 2009

J Atheroscler Thromb

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“…Reduction of postchallenge hyperglycemia by acarbose has been shown to prevent acute endothelial dysfunction [10,23], which prompted us to measure ADMA, an inhibitor of NO synthase causing reduced NO availability and thus endothelial dysfunction [24]. The time-dependent pattern of inhibition of sP-selectin by acarbose, in the face of unaltered levels of ADMA, is consistent with the hypothesis that the enhanced sPselectin in this setting largely originates from platelets rather than endothelial cells, and may therefore be considered an additional platelet activation marker.…”

Section: Discussionmentioning

confidence: 99%

“…The mechanism(s) by which glucose fluctuations during the postprandial period exert their deleterious effects may include enhanced oxidative stress and endothelial dysfunction, both of which contribute to platelet activation [3,9]. Treating patients with impaired glucose tolerance with acarbose, an a-glucosidase inhibitor that reduces postprandial hyperglycemia, prevents acute endothelial dysfunction [10] and may lower the risk of atherothrombotic events [11].…”

Section: Introductionmentioning

confidence: 99%

Postprandial hyperglycemia is a determinant of platelet activation in early type 2 diabetes mellitus

Santilli

Formoso

Sbraccia

et al. 2010

Journal of Thrombosis and Haemostasis

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Summary. Background: Chronic hyperglycemia is a major contributor to in vivo platelet activation in diabetes mellitus. Objectives: To evaluate the effects of acarbose, an a-glucosidase inhibitor, on platelet activation and its determinants in newly diagnosed type 2 diabetic patients. Methods: Forty-eight subjects (26 males, aged 61 ± 8 years) with early type 2 diabetes (baseline hemoglobin A 1c £ 7% and no previous hypoglycemic treatment) were randomly assigned to acarbose up to 100 mg three times a day or placebo, and evaluated every 4 weeks for 20 weeks. The main outcome measures were urinary 11-dehydro-thromboxane (TX)B 2 (marker of in vivo platelet activation) and 8-iso-prostaglandin (PG)F 2a (marker of in vivo lipid peroxidation) excretion rate, 2-h postprandial plasma glucose (PPG) after a test meal, and assessment of glucose fluctuations by mean amplitude of glycemic excursions (MAGE). Results: Baseline measurements revealed biochemical evidence of enhanced lipid peroxidation and platelet activation. As compared with the placebo group, patients treated with acarbose had statistically significant reductions in urinary 11-dehydro-TXB 2 and 8-iso-PGF 2a excretion rate as early as after 8 weeks and at each subsequent time point (between-group P < 0.0001 at 12, 16 and 20 weeks), following earlier decreases in PPG and MAGE. Multiple regression analyses in the acarbose group revealed that PPG was the only significant predictor of 11-dehydro-TXB 2 urinary excretion rate (b = 0.39, P = 0.002) and MAGE the only predictor of 8-iso-PGF 2a urinary excretion rate (b = 0.42, P = 0.001). Conclusions: Postprandial hyperglycemia is associated with enhanced lipid peroxidation and platelet activation in early type 2 diabetes. A moderate decrease in PPG achieved with acarbose causes time-dependent downregulation of these phenomena, suggesting a causal link between early metabolic abnormalities and platelet activation in this setting.

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“…The increase of blood glucose level (hyperglycemia) became the main factorto affecting endothelial dysfunction, which was the first criterion of atherosclerosis pathogenesis [25,26]. Endothelial dysfunction takes important role in the development of atherosclerosis, and the circulation of endothelial progenitor cells derived from the bone marrow participating in the repair of vascular endothelial cells and defending the function of endothelial.…”

Section: Vipalbumin ® Effect In Cd34 and Sdf-1 Mobilization In Streptmentioning

confidence: 99%

Detection of VipAlbumin® Effect in CD34 and SDF-1 Mobilization, in Streptozotocin-induced Diabetes Mellitus Mice

Pradana

Djati

Rifa’i

2015

JELS

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Diabetes mellitus is a disease in which the body loses its ability to provide tight regulation and maintain a dynamic interaction between the tissue sensitivity and insulin secretion by β cells. The impact of this dysfunctional mechanism is uncontrolled blood glucose levels that lead to hyperglycemia condition. Highly reactive free radicals have a strong involvement in the pathogenesis of diabetes mellitus, where one of its forming process may be triggered by hyperglycemia condition. Patients with diabetes mellitus itself vulnerable to endothelial dysfunction, which is caused by a decrease in circulating endothelial progenitor cells, and also a decrease in chemokines which play a role in affecting the activities of these cells. Hyperglycemia condition and free radical activity is a major cause of these endothelial progenitor cells dysfunction.The purpose of this study was to determine the role of VipAlbumin®, a supplement derived from Channa striatus albumin extracts in inhibiting the action of free radicals that are formed due to hyperglycemia condition, which can affect the increase in endothelial progenitor cells relative amount. This study used BALB/C mice that induced to undergo diabetes mellitus through streptozotocin injection intraperitoneally at 5-day old. Mice who have reached 4 week old and positive to diabetes mellitus (blood glucose levels > 200 mg.dl -1 ) will be administered with VipAlbumin® orally for 14 days. VipAlbumin® dosage was divided into 4 groups: positive control (without VipAlbumin®); 1 st dose (0.01664 mg.gr -1 BW); 2 nd dose (0.416 mg.gr -1 BW); 3 rd dose (10.4 mg.gr -1 BW). The last step was flow cytometric analysis to determine the development of endothelial progenitor cells relative amount, which isolated from bone marrow. The variables measured in this study were the relative amount of CD34 + and SDF-1. Based to flow cytometric analysis, mice with VipAlbumin® administration did not show any significant improvement in CD34 relative amount when compared to the positive control. Relative amount of Chemokine SDF-1 itself, although only occur at the 3 rd dose of VipAlbumin® treatment, has increased and significantly different from the positive control.

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Reduction of postchallenge hyperglycaemia prevents acute endothelial dysfunction in subjects with impaired glucose tolerance

Abstract: Our data clearly demonstrate that the postchallenge alteration of vascular function in patients with impaired glucose tolerance is caused by the acute elevation of glycaemia but not mediated by ADMA.

Cited by 76 publications

References 52 publications

Effects of Pitavastatin, a 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibitor, on Cardio-Ankle Vascular Index in Type 2 Diabetic Patients

Effects of Pitavastatin, a 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibitor, on Cardio-Ankle Vascular Index in Type 2 Diabetic Patients

Postprandial hyperglycemia is a determinant of platelet activation in early type 2 diabetes mellitus

Detection of VipAlbumin® Effect in CD34 and SDF-1 Mobilization, in Streptozotocin-induced Diabetes Mellitus Mice

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