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Journal ArticleDOI

Vascular Effects of Acute Hyperglycemia in Humans Are Reversed by l-Arginine Evidence for Reduced Availability of Nitric Oxide During Hyperglycemia

TLDR
The results show that acute hyperglycemia in normal subjects causes significant hemodynamic and rheological changes that are reversed by L-arginine, which suggests that hyper glycemia may reduce nitric oxide availability in humans.
Abstract
Background Acute hyperglycemia may increase vascular tone in normal humans via a glutathione-sensitive, presumably free radical–mediated pathway. The objective of this study was to investigate whether or not the vascular effects of hyperglycemia are related to reduced availability of nitric oxide. Methods and Results Acute hyperglycemia (15 mmol/L, 270 mg/dL) was induced in 12 healthy subjects with an artificial pancreas. Systolic and diastolic blood pressures, heart rate, and plasma catecholamines showed significant increases (P<.05) starting after 30 minutes of hyperglycemia; leg blood flow decreased significantly (15%; P<.05) at 60 and 90 minutes. Platelet aggregation to ADP and blood viscosity also showed significant increments (P<.05). The infusion of l-arginine (n=7, 1 g/min) but not d-arginine (n=5, 1 g/min) or l-lysine (n=5, 1 g/min) in the last 30 minutes of the hyperglycemic clamp completely reversed all hemodynamic and rheological changes brought about by hyperglycemia. Infusion of NG-monomethy...

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Journal ArticleDOI

Inflammation and Insulin Resistance

TL;DR: This is the first of two articles describing a symposium on insulin action, insulin resistance, inflammation, and Atherosclerosis in Niagara Falls, New York, 20–21 September 2002, which will cover topics related to atherosclerosis pathobiology and the cell biology of insulin resistance.
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Is Oxidative Stress the Pathogenic Mechanism Underlying Insulin Resistance, Diabetes, and Cardiovascular Disease? The Common Soil Hypothesis Revisited

TL;DR: In this paper, the authors proposed a pathogenic mechanism linking insulin resistance with dysfunction of both beta cells and endothelium, eventually leading to overt diabetes and cardiovascular disease, which may also contribute to explaining why treating cardiovascular risk with drugs, such as calcium channel blockers, ACE inhibitors, AT-1 receptor antagonists, and statins, all compounds showing intracellular preventive antioxidant activity, results in the onset of new cases of diabetes possibly being reduced.
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Management of diabetes and hyperglycemia in hospitals.

TL;DR: The purpose of this technical review is to evaluate the evidence relating to the management of hyperglycemia in hospitals, with particular focus on the issue of glycemic control and its possible impact on hospital outcomes.
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Oscillating glucose is more deleterious to endothelial function and oxidative stress than mean glucose in normal and type 2 diabetic patients

TL;DR: It is suggested that oscillating glucose can have more deleterious effects than constant high glucose on endothelial function and oxidative stress, two key players in favoring cardiovascular complications in diabetes.
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The role of oxidative stress in the onset and progression of diabetes and its complications: a summary of a Congress Series sponsored by UNESCO-MCBN, the American Diabetes Association and the German Diabetes Society.

TL;DR: This review summarises the results and discussions of an UNESCO‐MCBN supported symposium on oxidative stress and its role in the onset and progression of diabetes and suggests a role for ROI in the development of insulin resistance.
References
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Journal ArticleDOI

The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus.

TL;DR: Intensive therapy effectively delays the onset and slows the progression of diabetic retinopathy, nephropathy, and neuropathy in patients with IDDM.
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The L-Arginine-Nitric Oxide Pathway

TL;DR: The discovery that mammalian cells generate nitric oxide, a gas previously considered to be merely an atmospheric pollutant, is providing important information about many biologic processes.
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Vascular endothelial cells synthesize nitric oxide from L-arginine.

TL;DR: It is demonstrated that NO can be synthesized from L-arginine by porcine aortic endothelial cells in culture and the strict substrate specificity of this reaction suggests that L- arginine is the precursor for NO synthesis in vascular endothelium cells.
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Characterization of three inhibitors of endothelial nitric oxide synthase in vitro and in vivo

TL;DR: Results indicate that l‐NMMA, l‐NIO and l‐NAME are inhibitors of NO synthase in the vascular endothelium and confirm the important role of NO synthesis in the maintenance of vascular tone and blood pressure.
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Role of endothelium-derived nitric oxide in the regulation of blood pressure

TL;DR: Results indicate that nitric oxide formation from L-arginine by the vascular endothelium plays a role in the regulation of blood pressure and in the hypotensive actions of acetylcholine.
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