Glycosylated haemoglobin and plasma glycoprotein assays by affinity chromatography

Cardiovascular disease is responsible for most of the excess mortality associated with diabetes mellitus [1], and impaired endothelium-dependent relaxation has been described in humans and in animal models of the disease [2±6]. A variety of mechanisms have been proposed to explain this observation and, in particular, the role of nitric oxide (NO) has been evaluated. Nitric oxide production has been reported to be either increased [7] or decreased [8] in the presence of high glucose concentrations. Moreover, endothelial dysfunction following hyperglycaemia is associated with increased generation of oxygen free radicals [9] and vasoconstrictor prostanoids [10,11]. The observation that diabetes-induced abnormalities of vascular relaxation are reversed when the vessel segments are exposed to indomethacin in the organ Diabetologia (2000) Abstract Aims/hypothesis. Cardiovascular disease is the leading cause of death in diabetes mellitus. Abnormal endothelium-dependent relaxation is observed both in humans and in animal models of diabetes mellitus and decreased bioavailability of nitric oxide (NO) is thought to be involved in this defect. Therefore, the aim of this study was to test whether adenovirus-mediated gene transfer of endothelial nitric oxide synthase (eNOS) alters vascular reactivity of diabetic vessels. Methods. Vascular reactivity was first assessed in thoracic aortas and carotid arteries from nine alloxan-induced diabetic (plasma glucose, 26.5 ± 1.2 mmol/l; HbA 1 c , 6.4 ± 0.3 %) and nine control rabbits (plasma glucose, 11.1 ± 1.3 mmol/l; HbA 1 c , 2.1 ± 0.1 %). Vascular reactivity was next examined in thoracic aortas of diabetic animals after ex vivo transduction with replication-deficient adenovirus encoding gene for eNOS (AdeNOS) or b-galactosidase (Adbgal).Results. After 10 weeks of hyperglycaemia, endothelium-dependent relaxation to acetylcholine was impaired in diabetic aorta, but was normal in carotid arteries from diabetic rabbits. In contrast, responses of both vessels to calcium ionophore and nitric oxide donor were normal. Histochemical staining for b-galactosidase and immunohistochemistry for eNOS showed transgene expression in the endothelium and adventitia in Adbgal and AdeNOS transduced vessels, respectively. During submaximum contractions with phenylephrine, relaxations to low concentrations of acetylcholine (3 10 ±8 to 10 ±7 mol/l) were augmented in AdeNOS transduced diabetic vessels. Conclusion/interpretation. These findings suggest that adenovirus-mediated gene transfer of eNOS to diabetic aorta alters vascular reactivity. [Diabetologia (2000) 43: 340±347]

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“…Total plasma cholesterol and triglycerides were measured by standard techniques [19,20]. Total glycated haemoglobin was measured by HPLC [21].…”

Section: Methodsmentioning

confidence: 99%

Gene transfer of endothelial nitric oxide synthase alters endothelium-dependent relaxations in aortas from diabetic rabbits

et al. 2000

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“…Venous blood was sampled for serum electrolytes, creatinine, hemoglobin measurements (Cobas Mira analyser; Roche, Montclair, NJ), and HbA 1c by HPLC (CLC 330; Primus, Kansas City, MO), and urine was collected on three timed overnight nonconsecutive samples for calculation of ACR (Imunoturbidimetry Cobas Mira analyser) (25,26). GFR was calculated using the Cockroft-Gault formula (27).…”

Section: Designmentioning

confidence: 99%

Targeting Albumin Excretion Rate in the Treatment of the Hypertensive Diabetic Patient with Renal Disease

Krimholtz

Karalliedde²,

Thomas³

et al. 2005

Journal of the American Society of Nephrology

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Combination of an angiotensin-converting enzyme inhibitor (ACEI) with an angiotensin II receptor blocker is advocated as a treatment option in diabetic patients with nephropathy and residual albuminuria while on antihypertensive therapy. Abrogation of albuminuria is a key treatment goal to prevent disease progression. The assumption is that albuminuria reduction is the result of more complete blockade of the renin angiotensin system; thus, the ACEI-angiotensin II receptor blocker combination would have a greater albuminuria-lowering effect than the combination of an ACEI with a calcium channel blocker such as amlodipine, which causes similar reductions in BP but does not affect the renin angiotensin system. Twenty-eight patients who had type 1 diabetes and known diabetic renal disease and had a persistently elevated albumin creatinine ratio (ACR) >10 mg/mmol despite office BP recordings <140/80 mmHg on maximal recommended dose of the ACEI lisinopril were studied. Patients were allocated to receive either candesartan (16 mg/d) or amlodipine (10 mg/d) in addition to preexisting ACEI inhibition and followed for 24 wk in a randomized, double-blind, parallel-group trial. By week 24, ACR fell by 56% with candesartan and 54% with amlodipine (P < 0.01 versus baseline for both) with no significant difference between groups. Mean arterial BP fell between 3 and 6 mmHg similarly in both groups. In neither group was a significant correlation found between the change in ACR and the change in BP. Candesartan and amlodipine lowered ACR and BP by a similar degree. The fall in ACR was disproportionate to the fall of systemic BP and independent of it. The mechanism of the reduction in albuminuria seen with these agents in combination with an ACEI remains to be elucidated. M icroalbuminuria is a marker of renal disease in individuals both with and without diabetes and predicts cardiovascular disease (CVD) and early mortality (1-4). Although the terms normoalbuminuria, microalbuminuria, and macroalbuminuria (clinical albuminuria) describe different categories of albumin excretion rate (AER), it is important to recognize that the relationship between albumin excretion and cardiorenal risk is part of a continuum (1,3). There is a dose-response relationship between the degree of albuminuria and renal and cardiovascular risk that seems to rise at AER between 8 and 10 g/min, well below the level currently considered the upper boundary of the normal range of AER (1). Elevated rates of urinary albumin excretion predict target organ damage, notably renal disease, but are also related to left ventricular dysfunction, stroke, and myocardial infarction.The rates of progression of microalbuminuria to macroalbuminuria in recent times are approximately 45 to 50%, with 25 to 30% of patients remaining microalbuminuric over a 10-yr period. The regression rates to normoalbuminuria therefore are higher than described in previous decades (5-7). This changing natural history of microalbuminuria is a result of a number of factors that include improved gl...

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“…56 -58 Levels increase in patients with poorly controlled diabetes, and can be elevated despite normal concentrations of glycohemoglobin, consistent with the shorter circulating half-life of albumin relative to that of the erythrocyte. [59][60][61][62][63][64][65][66] Similarly, after resolution of a hyperglycemic episode, glycated albumin concentrations begin to fall before a diminution in the glycohemoglobin concentration is detectable. [67][68][69] Determination of glycated album in can complement and extend information provided by glycohemoglobin measurem ents, and may be particularly useful when early confirmation of response to recent changes in the therapeutic regimen is needed.…”

Section: Glycated Albumin and Glycated Plasma Proteinsmentioning

confidence: 99%

Measuring Glycated Proteins: Clinical and Methodological Aspects

Cohen¹,

Clements²

1999

Diabetes Technology & Therapeutics

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The recognition that nonenzymatic glycation, wherein free sugar condenses with certain reactive protein amino groups, is increased in hyperglycemic states has led to improved means for assessing diabetic control through the measurement of concentrations of glycated proteins in the circulation. This article reviews the chemistry, methods for measurement, and clinical relevance of circulating glycated proteins in the management of diabetes.

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Glycosylated haemoglobin and plasma glycoprotein assays by affinity chromatography

Cited by 60 publications

References 18 publications

Gene transfer of endothelial nitric oxide synthase alters endothelium-dependent relaxations in aortas from diabetic rabbits

Gene transfer of endothelial nitric oxide synthase alters endothelium-dependent relaxations in aortas from diabetic rabbits

Targeting Albumin Excretion Rate in the Treatment of the Hypertensive Diabetic Patient with Renal Disease

Measuring Glycated Proteins: Clinical and Methodological Aspects

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