Vascular methylglyoxal metabolism and the development of hypertension

Wang, Xiaoxia; Desai, Kaushik; Chang, Tuanjie; Wu, Lingyun

doi:10.1097/01.hjh.0000173778.85233.1b

Cited by 112 publications

(103 citation statements)

References 24 publications

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“…In our study, the postprandial circulating MG levels increased maximally at 4 h, an effect prevented by benfotiamine. Dicarbonyls can induce oxidative stress, promote inflammation (42), and induce endothelial apoptosis (43) and dysfunction (44).…”

Section: Correlationsmentioning

confidence: 99%

Benfotiamine Prevents Macro- and Microvascular Endothelial Dysfunction and Oxidative Stress Following a Meal Rich in Advanced Glycation End Products in Individuals With Type 2 Diabetes

et al. 2006

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OBJECTIVE -Diabetes is characterized by marked postprandial endothelial dysfunction induced by hyperglycemia, hypertriglyceridemia, advanced glycation end products (AGEs), and dicarbonyls (e.g., methylglyoxal [MG]). In vitro hyperglycemia-induced MG formation and endothelial dysfunction could be blocked by benfotiamine, but in vivo effects of benfotiamine on postprandial endothelial dysfunction and MG synthesis have not been investigated in humans until now.RESEARCH DESIGN AND METHODS -Thirteen people with type 2 diabetes were given a heat-processed test meal with a high AGE content (HAGE; 15.100 AGE kU, 580 kcal, 54 g protein, 17 g lipids, and 48 g carbohydrates) before and after a 3-day therapy with benfotiamine (1,050 mg/day). Macrovascular flow-mediated dilatation (FMD) and microvascular reactive hyperemia, along with serum markers of endothelial disfunction (E-selectin, vascular cell adhesion molecule-1, and intracellular adhesion molecule-1), oxidative stress, AGE, and MG were measured during both test meal days after an overnight fast and then at 2, 4, and 6 h postprandially.RESULTS -The HAGE induced a maximum reactive hyperemia decrease of Ϫ60.0% after 2 h and a maximum FMD impairment of Ϫ35.1% after 4 h, without affecting endotheliumindependent vasodilatation. The effects of HAGE on both FMD and reactive hyperemia were completely prevented by benfotiamine. Serum markers of endothelial dysfunction and oxidative stress, as well as AGE, increased after HAGE. These effects were significantly reduced by benfotiamine.CONCLUSIONS -Our study confirms micro-and macrovascular endothelial dysfunction accompanied by increased oxidative stress following a real-life, heat-processed, AGE-rich meal in individuals with type 2 diabetes and suggests benfotiamine as a potential treatment. Diabetes Care 29:2064 -2071, 2006E ndothelial dysfunction is an early marker of atherosclerosis and accompanies states showing a high cardiovascular risk, such as smoking (1), dyslipidemia (2), arterial hypertension (3), obesity (4), coronary artery disease (5), congestive heart failure (6), and type 1 (7) and type 2 (8) diabetes. Postprandial endothelial dysfunction has been proposed as the link between postprandial dysmetabolism and atherosclerosis (9) and occurs not only in patients with cardiovascular disease (10) or diabetes (11) but even in healthy subjects (12). Distinctive and cumulative (11) effects of hyperglycemia (13) and hypertriglyceridemia (14) on postprandial endothelial dysfunction have been shown. Since the postprandial state covers most of our daytime, interventions aimed at reducing postprandial endothelial dysfunction might play a decisive role in prevention of atherosclerosis. Several therapeutic approaches have been suggested for the treatment of postprandial endothelial dysfunction, including insulin, folic acid, tetrahydrobiopterin, vitamins C and E, and statins (11). These approaches aim at reducing postprandial oxidative stress (vitamins C and E, statins, and partly folic acid), postprandial hyperglycemia (insul...

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Section: Correlationsmentioning

confidence: 99%

Benfotiamine Prevents Macro- and Microvascular Endothelial Dysfunction and Oxidative Stress Following a Meal Rich in Advanced Glycation End Products in Individuals With Type 2 Diabetes

et al. 2006

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“…18 In any case, it is well established that oxidative stress is associated with arterial blood pressure increase, which may cause endothelial dysfunction and altered vascular reactivity. 19 According to this view, it is conceivable that a drug able to decrease IOP could also have a protective action on endothelial cells.…”

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confidence: 99%

Antioxidant activity of timolol on endothelial cells and its relevance for glaucoma course

Izzotti

Saccà²,

Marco

et al. 2007

Eye

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Purpose A growing evidence in the scientific literature suggests that oxidative damage plays a pathogenic role in primary open-angle glaucoma. Therefore, it is of interest to test whether drugs effective against glaucoma display antioxidant activity. We test the hypothesis that the classic b-blocker therapy for glaucoma with timolol involves the activation of antioxidant protective mechanisms towards endothelial cells. Methods Oxidative stress was induced in cultured human endothelial cells by iron/ ascorbate with or without timolol pretreatment. Analysed parameters included cell viability (neutral red uptake and tetrazolium salt tests), lipid peroxidation (thiobarbituric reactive substances), and occurrence of molecular oxidative damage to DNA (8-hydroxy-2 0 -deoxyguanosine).Results Oxidative stress decreased 1.8-fold cell viability, increased 3.0-fold lipid peroxidation and 64-fold oxidative damage to DNA. In the presence of timolol, oxidative stress did not modify cell viability, whereas lipid peroxidation was increased 1.3-fold, and DNA oxidative damage 3.6-fold only.Conclusions The obtained results indicate that timolol exerts a direct antioxidant activity protecting human endothelial cells from oxidative stress. These cells employ mechanisms similar to those observed in the vascular endothelium. It is hypothesized that this antioxidant activity is involved in the therapeutic effect of this drug against glaucoma.

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“…MG has been postulated to play a role in the development of hypertension [36]. Studies using animal model and cell cultures showed a significant increase in blood pressure to coincide with elevated MG level in plasma and aortic tissues [37], [38]. However, functional links between MG biogenesis and hypertension, in part mediated by ROS and AGEs, have only been documented in rat model but not yet in humans under these conditions.…”

Section: Resultsmentioning

confidence: 99%

Oxidative Stress and Kidney Glycation in Rats Exposed Cadmium

Suhartono¹

2014

IJCEA

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Abstract-Cadmium (Cd) is a heavy metal and it was proposed in the formation of Reactive Oxygen Species (ROS) and Advance Glycation End Products (AGEs). The role of Cd induced oxidative stress and glycation in kidney has not been much studied. Thus our study aimed to measure the oxidative stress and glycation in kidney exposed to Cd. The present study was a true experimental study design to examine the impact of Cd exposure in renal rats (Rattus novergicus) male. The study involved 4 groups, K0 was the control group, while the other (K1,K2,K3) was the case group with exposure of Cd in different concentration. For analyzing of the data, SPSS software version 17 was used and was examined by ANOVA test. The resulted showed that there are a significance differences of MDA, H 2 O 2, SOD activity and AOPP between case and control group, but there are not MG and CC are not sgnificance differences. Our study showed Cd induced oxidative stress but not caused glycation reaction.Index Terms-AOPP, cadmium, glycation and oxidative stress.

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Vascular methylglyoxal metabolism and the development of hypertension

Abstract: Increased aortic MG, AGE formation and oxidative stress were associated with blood pressure increase in SHR, which may cause endothelial dysfunction and altered vascular reactivity.

Cited by 112 publications

References 24 publications

Benfotiamine Prevents Macro- and Microvascular Endothelial Dysfunction and Oxidative Stress Following a Meal Rich in Advanced Glycation End Products in Individuals With Type 2 Diabetes

Benfotiamine Prevents Macro- and Microvascular Endothelial Dysfunction and Oxidative Stress Following a Meal Rich in Advanced Glycation End Products in Individuals With Type 2 Diabetes

Antioxidant activity of timolol on endothelial cells and its relevance for glaucoma course

Oxidative Stress and Kidney Glycation in Rats Exposed Cadmium

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