A novel method for the rapid separation of plasma lipoproteins using self-generating gradients of iodixanol

Graham, John M.; Higgins, Joan A.; Gillott, T.; Taylor, T.; Wilkinson, Jane; Ford, Terence C.; Billington, David C.

doi:10.1016/0021-9150(96)05797-8

Cited by 84 publications

(69 citation statements)

References 11 publications

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“…18 LDL-C was calculated after lipoprotein separation. 19 Plasma glucose was measured by the glucose-oxidase method and HbA1c by high-performance liquid chromatography. Nitrotyrosine plasma concentration was assayed by ELISA.…”

Section: Biochemical Measurementsmentioning

confidence: 99%

Evidence for an Independent and Cumulative Effect of Postprandial Hypertriglyceridemia and Hyperglycemia on Endothelial Dysfunction and Oxidative Stress Generation

et al. 2002

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Background-Postprandial hypertriglyceridemia and hyperglycemia are considered risk factors for cardiovascular disease.Evidence suggests that postprandial hypertriglyceridemia and hyperglycemia induce endothelial dysfunction through oxidative stress; however, the distinct role of these two factors is a matter of debate. Methods and Results-Thirty type 2 diabetic patients and 20 normal subjects ate 3 different meals: a high-fat meal; 75 g glucose alone; and high-fat meal plus glucose. Glycemia, triglyceridemia, nitrotyrosine, and endothelial function were assayed during the tests. Subsequently, diabetics took 40 mg/d simvastatin or placebo for 12 weeks. The 3 tests were performed again at baseline, between 3 to 6 days after the start, and at the end of each study. High-fat load and glucose alone produced a decrease of endothelial function and an increase of nitrotyrosine in normal and diabetic subjects. These effects were more pronounced when high fat and glucose were combined. Short-term simvastatin treatment had no effect on lipid parameters but reduced the effect on endothelial function and nitrotyrosine observed during each different test. Long-term simvastatin treatment was accompanied by a lower increase in postprandial triglycerides, which was followed by smaller variations of endothelial function and nitrotyrosine during the tests. Conclusions-This study shows an independent and cumulative effect of postprandial hypertriglyceridemia and hyperglycemia on endothelial function, suggesting oxidative stress as common mediator of such effect. Simvastatin shows a beneficial effect on oxidative stress and endothelial dysfunction, which may be ascribed to a direct effect as well as the lipid-lowering action of the drug.

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Section: Biochemical Measurementsmentioning

confidence: 99%

Evidence for an Independent and Cumulative Effect of Postprandial Hypertriglyceridemia and Hyperglycemia on Endothelial Dysfunction and Oxidative Stress Generation

et al. 2002

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“…21 LDL cholesterol was calculated after lipoprotein separation. 22 Plasma glucose was measured by the glucose-oxidase method, and HbA1c was assessed by high-performance liquid chromatography. NT was measured by ELISA as previously described.…”

Section: Biochemical Measurementsmentioning

confidence: 99%

Effect of Atorvastatin and Irbesartan, Alone and in Combination, on Postprandial Endothelial Dysfunction, Oxidative Stress, and Inflammation in Type 2 Diabetic Patients

et al. 2005

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Background-Postprandial hypertriglyceridemia and hyperglycemia are considered risk factors for cardiovascular disease.Evidence suggests that postprandial hypertriglyceridemia and hyperglycemia induce endothelial dysfunction and inflammation through oxidative stress. Statins and angiotensin type 1 receptor blockers have been shown to reduce oxidative stress and inflammation, improving endothelial function. Methods and Results-Twenty type 2 diabetic patients ate 3 different test meals: a high-fat meal, 75 g glucose alone, and a high-fat meal plus glucose. Glycemia, triglyceridemia, endothelial function, nitrotyrosine, C-reactive protein, intercellular adhesion molecule-1, and interleukin-6 were assayed during the tests. Subsequently, diabetics took atorvastatin 40 mg/d, irbesartan 300 mg/d, both, or placebo for 1 week. The 3 tests were performed again between 5 and 7 days after the start of each treatment. High-fat load and glucose alone produced a decrease in endothelial function and increases in nitrotyrosine, C-reactive protein, intercellular adhesion molecule-1, and interleukin-6. These effects were more pronounced when high-fat load and glucose were combined. Short-term atorvastatin and irbesartan treatments significantly counterbalanced these phenomena, and their combination was more effective than either therapy alone. Conclusions-This study confirms an independent and cumulative effect of postprandial hypertriglyceridemia and hyperglycemia on endothelial function and inflammation, suggesting oxidative stress as a common mediator of such an effect. Short-term treatment with atorvastatin and irbesartan may counterbalance this phenomenon; the combination of the 2 compounds is most effective.

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“…HDL cholesterol was estimated after precipitation of apolipoprotein B with phosphotungstatemagnesium (13). LDL cholesterol was calculated after lipoprotein separation (14). Plasma glucose was measured by the glucose oxidase method and A1C by highperformance liquid chromatography.…”

Section: Biochemical Measurementsmentioning

confidence: 99%

Simultaneous Control of Hyperglycemia and Oxidative Stress Normalizes Endothelial Function in Type 1 Diabetes

Ceriello

Kumar

Piconi³

et al. 2007

Diabetes Care

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OBJECTIVE -Previous studies have shown that in type 1 diabetes endothelial dysfunction persists even when glycemia is normalized. Moreover, oxidative stress has recently been demonstrated to be the mediator of hyperglycemia-induced endothelial dysfunction.RESEARCH DESIGN AND METHODS -Thirty-six type 1 diabetic patients and 12 control subjects were enrolled. The diabetic patients were divided into three groups. The first group was treated for 24 h with insulin, achieving a near-normalization of glycemia. After 12 h of this treatment, vitamin C was added for the remaining 12 h. The second group was treated for 24 h with vitamin C. After 12 h of this treatment, insulin was started, with achievement of near-normalization of glycemia for the remaining 12 h. The third group was treated for 24 h with both vitamin C and insulin, achieving near-normalization of glycemia.RESULTS -Neither normalization of glycemia nor vitamin C treatment alone was able to normalize endothelial dysfunction or oxidative stress. However, a combination of insulin and vitamin C normalized endothelial dysfunction and decreased oxidative stress to normal levels.CONCLUSIONS -This study suggests that long-lasting hyperglycemia in type 1 diabetic patients induces permanent alterations in endothelial cells, which may contribute to endothelial dysfunction by increased oxidative stress even when hyperglycemia is normalized. Diabetes Care 30:649 -654, 2007T ype 1 diabetes is associated with increased incidence of macrovascular diseases (1).The accelerated macrovascular disease is due in part to the increased incidence of classic risk factors, such as hypertension and dyslipidemia (2). However, recent evidence suggests that hyperglycemia also plays a significant role (3).The endothelium is a major organ involved in the development of cardiovascular disease, even in diabetes (4). All risk factors involved in the pathogenesis of cardiovascular disease, such as dyslipidemia and hypertension, can induce endothelial dysfunction, which has largely been shown to be predictive of a future cardiovascular event (4).The presence of endothelial dysfunction has often been reported in diabetes (4). However, whereas several studies have shown that hyperglycemia induces endothelial dysfunction in both diabetic and nondiabetic subjects (5-7), a clear demonstration that control of hyperglycemia can restore/normalize endothelial function is still lacking. In particular, in type 1 diabetic patients endothelial dysfunction has been reported to be present even when normoglycemia was achieved (8,9). Furthermore, several studies indicated that hyperglycemia induces endothelial dysfunction through the generation of oxidative stress (for review, see ref. 10), which has been suggested to be the key player in the generation of diabetes complications, both micro-and macrovascular (11). Therefore, the aim of this study was to evaluate the distinct as well as the combined effect of controlling hyperglycemia and oxidative stress on endothelial function in type 1 diabetic patients. RESE...

show abstract

A novel method for the rapid separation of plasma lipoproteins using self-generating gradients of iodixanol

Cited by 84 publications

References 11 publications

Evidence for an Independent and Cumulative Effect of Postprandial Hypertriglyceridemia and Hyperglycemia on Endothelial Dysfunction and Oxidative Stress Generation

Evidence for an Independent and Cumulative Effect of Postprandial Hypertriglyceridemia and Hyperglycemia on Endothelial Dysfunction and Oxidative Stress Generation

Effect of Atorvastatin and Irbesartan, Alone and in Combination, on Postprandial Endothelial Dysfunction, Oxidative Stress, and Inflammation in Type 2 Diabetic Patients

Simultaneous Control of Hyperglycemia and Oxidative Stress Normalizes Endothelial Function in Type 1 Diabetes

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