A rapid method for the determination of glycosylated hemoglobins using high pressure liquid chromatography

Cole, Richard; Soeldner, J S; Dunn, Peter J.; Bunn, H. Franklin

doi:10.1016/0026-0495(78)90109-9

Cited by 185 publications

(62 citation statements)

References 22 publications

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“…The one proviso to this is the need for greater care in sample handling for there is a progressive increase in the Hb AI~+b fraction with time [22] unless this is obviated by storage at -80 ~ or prompt analysis of the samples. With present technology, however, Hb A~ can be determined in approximately ten minutes per sample [16] and accordingly this method is feasible for routine clinical application.…”

Section: Discussionmentioning

confidence: 99%

“…Hb Aic% and Hb AI% were determined with a high performance liquid chromatography technique [16]. Aliquots of a pooled haemolysate were kept in liquid nitrogen and run at the beginning and end of each day's samples.…”

Section: Methodsmentioning

confidence: 99%

“…Aliquots of a pooled haemolysate were kept in liquid nitrogen and run at the beginning and end of each day's samples. The inter-and intra-run coeffidents of variation of the quality control sample were both approximately 3% [16]. Serum cholesterol and serum triglycerides were measured with an automated colorimetric method [ 17], and serum growth hormone by radioimmunoassay [18].…”

Section: Methodsmentioning

confidence: 99%

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Temporal relationship of glycosylated haemoglobin concentrations to glucose control in diabetics

et al. 1979

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Summary. To examine the temporal relationship between Hb Aic values and various indices of blood glucose control, 38 diabetic and 28 nondiabetic youth counsellors employed at two summer camps for diabetic children took part in an eight-week study. Each week fasting determinations were made of Hb AI, Hb Al~ , serum cholesterol, triglyceride and growth hormone and plasma glucose. Total daily urine glucose excretion was measured approximately two times per week, capillary glucose values were measured fasting and at 11 a. m. and 3 p. m. on two days per week, and urine glucose was measured semiquantitatively four times per day. As Hb AI was correlated highly with Hb AI0 (r = 0.997), it was used as the primary index of glycosylated haemoglobin. The mean values of Hb AI, serum cholesterol and triglycerides and fasting plasma glucose were all significantly elevated in the diabetic group but only Hb AI values provided total separation of the two groups. Within the diabetic group the Week 8 Hb A I values showed a significant correlation with the Week 8 mean capillary glucose concentrations, the proportion of urine tests showing 2% and 0% glycosuria, and mean serum triglycerides. Correlations of Week 8 Hb A~ with the mean values of these glycaemic parameters for each week of the study demonstrated low order correlations with the glycaemie measures of Week 1, and a progressive increase in the degree of correlation reaching a plateau with the glycaernic measures of Week 4 to 8. Similar correlation analysis using the Hb Ai values from Week 4 confirmed these findings. Therefore, while Hb AI provides an index of the control of diabetes, it appears to be more acutely responsive to blood glucose alteration than generally recognized.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Temporal relationship of glycosylated haemoglobin concentrations to glucose control in diabetics

et al. 1979

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“…Fasting plasma glucose concentration was measured by the glucose oxidase method and haemoglobin A 1c (HbA 1 c ) was determined by HPLC [23]. Serum and urinary creatinine were measured by the Jaffe reaction [24].…”

Section: Methodsmentioning

confidence: 99%

Protein C activation in NIDDM patients

et al. 1996

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Alteration of the clotting system in diabetic patients is presently the focus of increasing interest due to its potential role in the pathogenesis of large and smallvessel disease in diabetes mellitus. It is believed that enhanced pro-coagulant activity is linked to the excessive cardiovascular morbidity and mortality among diabetic patients which have not been fully explained by major risk factors such as arterial hypertension, cigarette smoking and hypercholesterolaemia. Perturbance of haemostasis has also been implicated in the development of complications such as nephropathy and retinopathy and in the acceleration of atherogenesis observed in diabetic patients [1,2]. Diabetologia (1996Diabetologia ( ) 39: 1455Diabetologia ( -1461 Protein C activation in NIDDM patients Summary Enhanced activation of the clotting system has been recently implicated in the pathogenesis of vascular complications in patients with diabetes mellitus. Abnormalities of the anticoagulant system may constitute a potential trigger factor for the haemostatic activation observed in diabetic subjects. The current study aimed to evaluate anticoagulant activity in diabetic patients by assessing the plasma levels of activated protein C-protein C inhibitor complex; and by measuring the anticoagulant response to exogenous thrombomodulin. This study comprised 61 patients (34 men, 27 women) with non-insulin-dependent diabetes mellitus (NIDDM) of whom 22 showed microalbuminuria and 39 normoalbuminuria. Data obtained in 31 non-obese and non-diabetic subjects were available for comparison. The plasma levels of fibrinogen (p < 0.02), prothrombin fragment 1 + 2 (p < 0.05), fibrin monomer (p < 0.0001), protein C antigen (p < 0.005), total protein S antigen (p < 0.02), soluble thrombomodulin (p < 0.005) and soluble Eselectin (p < 0.005) were significantly higher in diabetic patients than in healthy subjects. The plasma level of activated protein C-protein C inhibitor complex (7.4 ± 3.8 vs 3.0 ± 0.4 pmol/l) was significantly higher (p < 0.0001) and the anticoagulant response to exogenous thrombomodulin (23.4 ± 2.6 vs 35.3 ± 3.0 ng/ml) was markedly lower (p = 0.005) in all diabetic patients than in healthy subjects. Cases with microalbuminuria presented low plasma levels of activated protein C-protein C inhibitor complex (5.5 ± 0.6 vs 8.6 ± 0.7 pmol/l, p < 0.05) and significantly decreased values of the anticoagulant response to exogenous thrombomodulin (16.5 ± 2.9 vs 23.4 ± 2.6 %, p = 0.03) as compared to those with normoalbuminuria. The present study suggests that the hyper-coagulable state in NIDDM is associated with an increased activation of protein C but with a poor plasma reactivity to the anticoagulant effect of thrombomodulin.

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“…An exponential function was used with constant p1 representing the fractional decrease in input per unit time (hours). t denotes the value at time t, t0 the value at zero time Richmond, Calif., USA) [21]. Serum free insulin concentrations were determined by double antibody radioimmunoassay (Pharmacia Insulin RIA Kit; Pharmacia, Uppsala, Sweden) after precipitation with polyethylene glycol.…”

Section: Kinetic Analysis Of Vldl1 and Vldl2 Apo Bmentioning

confidence: 99%

Defective regulation of triglyceride metabolism by insulin in the liver in NIDDM

et al. 1997

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Features of diabetic dyslipidaemia in non-insulin-dependent diabetes mellitus (NIDDM), such as a low HDL cholesterol concentration, the preponderance of small dense LDL and postprandial fat intolerance are considered to be metabolic consequences of elevated plasma triglycerides [1]. The mechanism underlying hypertriglyceridaemia in NIDDM is still unclear. A majority of studies indicate that the elevation of plasma triglycerides in NIDDM result from an overproduction of VLDL triglyceride [2,3] and apo B [4,5] but it is unclear and a matter of controversy whether the increased production of VLDL particles is driven by a direct effect of hyperinsulinaemia or is a consequence of defective suppression of VLDL production by insulin [1]. In healthy subjects acute insulin administration suppresses VLDL apo B production [6][7][8]. Data on the suppression of VLDL production by insulin in insulin resistant states are controversial. Lewis et al. [6] showed an impaired suppression of VLDL apo B production in obese subjects while Cummings et al. [9] did not find any defect in the ability of insulin to suppress VLDL apo B production in patients with NIDDM.Two major subclasses of VLDL particles are recognised, large triglyceride-rich VLDL1 particles Diabetologia (1997) 40: 454-462 Defective regulation of triglyceride metabolism by insulin in the liver in NIDDM Summary Insulin administration to healthy subjects inhibits the production of very low density lipoprotein (VLDL)1 (Svedbergs flotation (Sf) rate 60-400) without affecting that of VLDL2 (Sf 20-60) subclass. This study was designed to test whether this hormonal action is impaired in non-insulin-dependent diabetes mellitus (NIDDM). We studied six men with NIDDM (age 53 ± 3 years, body mass index 27.0 ± 1.0 kg/m 2 , plasma triglycerides 1.89 ± 0.22 mmol/l) during an 8.5 h infusion of saline (control) and then in hyperinsulinaemic (serum insulin ∼ 540 pmol/l) conditions during 8.5 h infusions of glucose and insulin to give either hyper-and normoglycaemic conditions. [3-2 H]-leucine was used as tracer and kinetic constants derived using a non-steadystate multicompartmental model. Compared to the control study, patients with NIDDM reduced VLDL1 apo B production by only 3 ± 8 % after 8.5 h of hyperinsulinaemia (701 ± 102 vs 672 ± 94 mg/day respectively, NS) in hyperglycaemic conditions and by 9 ± 21 % under normoglycaemic conditions (603 ± 145 mg/day). In contrast, in normal subjects insulin induced a 50 ± 15 % decrement in VLDL1 apo B production (p < 0.05). Direct synthesis of VLDL2 apo B in patients with NIDDM was not markedly affected by insulin. We conclude that a contributory factor to hypertriglyceridaemia in NIDDM is the inability of insulin to inhibit acutely the release of VLDL1 from the liver, despite efficient suppression of serum nonesterfied fatty acids. [Diabetologia (1997) 40: 454-462]

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A rapid method for the determination of glycosylated hemoglobins using high pressure liquid chromatography

Cited by 185 publications

References 22 publications

Temporal relationship of glycosylated haemoglobin concentrations to glucose control in diabetics

Temporal relationship of glycosylated haemoglobin concentrations to glucose control in diabetics

Protein C activation in NIDDM patients

Defective regulation of triglyceride metabolism by insulin in the liver in NIDDM

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