A Simple Microchromatographic Column for Determination of Hemoglobins A1a+b and A1c

A simple microchromatographic homemade column was devised for the measurement of glycosylated minor hemoglobin fractions. the mean and one standard deviation of hemoglobins A_1a+b,A_1c and A_1a+b+c determined by the homemade column in 150 non-diabetic controls and 56 juvenile onset insulin-dependent diabetics were 2.6 + 0.5%, 6.0 + 1.0%, 8.6 + 1.1%, 3.3 + 0.9%, 13.7 + 2.2% and 16.9 + 2.8% respectively. A twofold increase in hemoglobins A_1c and A_1a+b+c levels was observed in the diabetics as compared to the non-diabetic controls suggesting that the homemade column is valid for the measurement of all three glycosylated hemoglobin fractions and assessment of blood glucose control in diabetic patients. the homemade column procedure yields accurate and reproducible results, is simple to perform, inexpensive, relatively rapid and may be used in the routine clinical laboratory. Hemoglobin A_1a+b+c levels measured by a commercial column in 35 non-diabetic controls and in 56 diabetics showed good correlation (R=0.91) with hemoglobin A_1a+b+c levels determined by the homemade column. the commercial column is valid for the measurement of the combined glycosylated hemoglobin A_1a+b+c fraction and may be used in the routine clinical laboratory to assess diabetic control.     

Serum adiponectin concentrations are not related to glycosylated hemoglobin levels (HbA1c) in obese diabetic and non-diabetic caucasians.

Although circulating adiponectin has been inversely correlated with obesity, type 2 diabetes and serum glycosylated hemoglobin (HbA1c) in humans, contradictory reports on that subject exist. In this study, serum concentrations of adiponectin in obese non-diabetic and diabetic humans were measured to examine whether they were associated with levels of HbA1c. The WHO definitions of obesity and diabetes were used. One hundred and five obese euglycemic subjects and 49 obese diabetics (aged 51+/-6.9, and 52+/-6.7 years, respectively) were studied. Their BMI, HbA1c and % of body fat were measured. Adiponectin was determined by an enzyme-linked immunosorbent assay. Although the serum adiponectin concentrations differed between diabetics and non-diabetics ( P<0.01), they were not correlated with HbA1c (r=-0.0814; P=0.5823, and r=-0.1861; P=0.1099, for diabetics and non-diabetics, respectively). Both diabetics and non-diabetics were segregated into tertiles according to their HbA1c levels. Plasma adiponectin did not differ significantly between the high (H), intermediate (I), and low (L) HbA1c tertiles. CONCLUSION: Concentrations of adiponectin were not correlated with levels of glycosylated hemoglobin in the diabetic and non-diabetic subjects examined.     

The usefulness of a rapid method for total fast hemoglobins determination in screening for diabetes control

We have used a simple and rapid method for the determination of total fast hemoglobins (HbA1a+b+c) in 102 diabetics and 36 normal controls. The method was described by Kynoch and marketed by Isolab. It proved to be useful in screening for patients with inadequate metabolic control in whom as a rule, total fast Hb values were higher than 8.5%. Mean Hb A1a+b+c value was significantly higher in the group of diabetics in comparison with normals (9.9 +/- 0.2 versus 6.9 +/- 0.8%). The diabetic patients were separated into four groups according to predetermined criteria of recent metabolic control. Even the patients considered to have a very good diabetes control during the past eight weeks, had supranormal total fast Hb values (7.7 +/- 0.2%). In the patients with good, poor and bad diabetes control, mean total fast Hb levels were respectively 9.3 +/- 0.3, 10.1 +/- 0.3 and 12.5 +/- 0.4%. In normals, there was a positive correlation between individual fasting blood glucose and total fast Hb values and in diabetics, mean blood glucose values correlated with total fast Hb levels. Hb A1a+b+c determinations also correlated with triglyceride values. We could find no significant association between high total fast Hb levels (greater than 8.5%) and the prevalence of retinopathy.     

A rapid micro-scale method for the measurement of haemoglobin A1(a+b+c)

Summary A rapid method is described for the measurement of total glycosylated haemoglobins (HbA_1(a+b+c). The procedure utilizes 0.05 ml of blood and takes forty minutes to complete manually. Eighty blood samples can be analysed without automation by one person in a day. Each analysis uses less than 2 mg of potassium cyanide, resulting in a method that is both safe and rapid for routine hospital laboratories. The inter-assay coefficient of variation was 4% and that for intra-assay measurements 3%, over the range 5–20% HbA_1(a+b+c). The method confirmed that the level of HbA_1(a+b+c) is elevated in imperfectly controlled diabetics. Amongst patients with blood glucose levels of less than 10 mmol/l the mean level of HbA_1(a+b+c) was found to be 8.5%; samples from 14 known diabetics gave a mean value of 10.9%, whereas 17 known non-diabetic samples gave a mean value of 8.3%. In the group of samples from 27 diabetic individuals with blood glucose levels above 10 mmol/l the mean level of HbA_1(a+b+c) was found to be 13.5%.     

Modification of Hemoglobin by Acetaldehyde: A Time Course Study by High Pressure Liquid Chromatography

Acetaldehyde forms stable adducts with proteins, and rapidly eluting hemoglobins on cation exchange chromatography have been found to be elevated in persons consuming excess alcohol. Incubation of hemoglobin hemolysate with 5 mM acetaldehyde at 37°C for various time intervals resulted in linear increases in the amounts of hemoglobin (Hb)A1a+b and HbA1c fractions determined by cation exchange high pressure liquid chromatography. The rate of formation of the HbA1c fraction was significantly higher (p < 0.001) than that of the HbA1a+b fraction. No increases in the amounts of minor hemoglobins were observed when hemoglobin was incubated with 0.05 mM acetaldehyde. Incubation of hemoglobin with 5 m acetaldehyde followed by reduction with sodium borohydride (NaBH₄.) resulted in a significant increase in both HbA1a+b and HbA1c fractions. The rate of formation of the HbA1c fraction was again significantly faster than that of HbA1a+b. Dialysis of nonreduced acetaldehyde- modified hemoglobin had no effect on the amounts of the two minor hemoglobin fractions. Dialysis of NaBH₄-reduced acetaldehyde-modified hemoglobin resulted in decreased amounts of the HbA1a+b fractions but no changes in the HbAlc fractions. Incubation with sodium cyanoborohydride led to minimal changes in chromatographic properties of hemoglobin. The clinical utility of acetaldehyde-modified hemoglobin eluting in the HbA1c fraction in the detection of excess alcohol consumption appears to be limited by the high concentration of acetaldehyde required. Furthermore, attempts to stabilize acetaldehyde-Schiff base adducts of hemoglobin with reducing agents must include appropriate controls, since the reductive step alone may lead to changes in the chromatographic properties of hemoglobin.     

Serum IgA levels in patients with diabetic nephropathy and IgA nephropathy superimposed on diabetes mellitus

The aim of this study was to examine the relationship between serum immunoglobulin A (IgA) levels and diabetic nephropathy in patients with type 2 diabetes mellitus, and to describe the role of IgA nephropathy superimposed on diabetes mellitus. A total of 127 type 2 diabetic patients were studied. Of these diabetics, 74 had no proteinuria, 35 had diabetic glomerulosclerosis confirmed by renal biopsy, 13 had superimposed IgA nephropathy, and five had superimposed non-IgA nephropathy. We also studied 93 non-diabetic patients with IgA nephropathy, 24 non-diabetic patients with non-IgA nephropathy, and 38 non-diabetic controls. Serum IgA levels were significantly higher in IgA nephropathy patients (350+/-130 mg/dl) than in non-diabetic controls (228+/-56 mg/dl) and diabetics without proteinuria (268+/-104 mg/dl). Serum IgA levels were also significantly higher in diabetics with superimposed IgA nephropathy (470+/-208 mg/dl) than in non-diabetic controls, non-IgA nephropathy patients (270+/-133 mg/dl), diabetics without proteinuria, diabetic glomerulosclerosis alone (302+/-126 mg/dl), and diabetics with superimposed non-IgA nephropathy (248+/-137 mg/dl). The prevalence of high serum IgA levels was significantly higher in diabetics with superimposed IgA nephropathy (76.9%) than in diabetic glomerulosclerosis alone (31.4%) and diabetics with superimposed non-IgA nephropathy (25.0%). In conclusion, our findings indicate that high serum IgA level is a sign of the existence of IgA nephropathy superimposed on diabetes mellitus.     

The association between heart rate and glycemia in adult diabetic subjects

We have studied the association between heart rate and glycemia in 221 diabetic and 109 non-diabetic adult subjects. Supine and standing heart rates were both statistically significantly higher (P less than 0.001) in the diabetic patients than in the control subjects. Among the diabetics, both the supine and standing heart rates were positively associated with hemoglobin A1c (r = 0.26, P less than 0.001 and r = 0.27, P less than 0.001 respectively). Patients with hemoglobin A1c values greater than 10.00% had a mean heart rate of 84.2 +/- 2.4, while those with hemoglobin A1c values less than 6.00% had a mean of 74.0 +/- 1.5 (P less than 0.001). The associations between heart rate and hemoglobin A1c persisted (P less than 0.001) with allowances for potential confounding variables in multiple regression analyses. The 15:30 difference, an indicator of parasympathetic function, was not associated with either heart rate or glycemia. These data suggest that the heart rate elevation in adult diabetic patients is the result of metabolic abnormalities.     

Angiotensin-converting enzyme and diabetes mellitus

Elevation of serum angiotensin-converting enzyme (ACE) has been reported to occur in 25 p. 100 of diabetic patients. This finding would decrease the specificity of increased ACE level in sarcoidosis. We measured serum ACE in 90 diabetic patients with simultaneous analysis of various parameters including those appreciating the degree of metabolic control. Serum ACE values, observed in diabetics are not different from values measured in controls, respectively 22,3 +/- 6,4 and 21,1 +/- 6,7 U/ml (means +/- SD). Only 5,5 p. 100 of diabetic patients had (slightly) increased serum ACE levels, i.e.: levels above mean +/- 2 SD of values observed in controls. Serum ACE levels were higher in insulin-dependent diabetics: 24,7 +/- 6,7 (n = 34) than in non insulin-dependent diabetics: 20,8 +/- 5,9 (n = 56) (p = 0,01). In the diabetic group, there is a positive linear correlation between serum ACE level and 24h-glycosuria or glycosylated A1c hemoglobin. These are parameters appreciating middle or long-term metabolic control. In the other hand, no correlation was observed between serum ACE and glycemia, triglyceridemia, serum creatinin, blood pressure or the presence of diabetic retinopathy. These findings do not show an elevation of serum ACE in diabetic patients. However, they suggest that long-term metabolic control of diabetes influence serum ACE level.     

Hemoglobin A1 correlates with the ratio of low-to high-density-lipoprotein cholesterol in normal weight type II diabetics

Because cardiovascular risk correlates with serum low density lipoprotein (LDL) cholesterol and is inverse with high density lipoprotein (HDL) cholesterol, the LDL-HDL cholesterol ratio has been advocated as a sensitive index of relative cardiovascular risk. In 50 normal weight insulin-treated Type II diabetic subjects, mean LDL-HDL ratios were significantly higher than for controls. In diabetic women, the LDL-HDL cholesterol ratio correlated with hemoglobin A1 better than any of the lipids or lipoprotein cholesterol fractions. When 8 poorly controlled diabetics were treated with insulin, the LDL-HDL ratio changed more significantly than did its component fractions, and the fall in LDL-HDL ratio paralleled the fall in hemoglobin A1.     

Mean platelet volume in Type 2 diabetic patients

BACKGROUND: Altered platelet morphology and function have been reported in patients with diabetes mellitus. They are likely to be associated with the pathological processes and increased risk of vascular disease seen in these patients. We aimed to determine the mean platelet volume (MPV) in diabetics compared to nondiabetics, to see if there is a difference in MPV between diabetics with and without macro- and microvascular complications, and to determine the correlation between MPV and fasting blood glucose, glycosylated hemoglobin (HbA(1)c), patient age, and duration of diabetes, respectively. METHODS: We measured MPV in 145 consecutive Type 2 diabetic patients and 100 nondiabetic control subjects without known coronary artery disease who had complete blood count on venous blood sample taken into tripotassium EDTA, using a Roche Minos cell counter and automatic blood counter (CELL-DYN 3500). The blood glucose level was measured by glucose oxidase method and HbA1c by calorimetrical method in the autoanalyser. Statistical evaluation was performed by SPSS for Windows statistics programme using multivariate logistical regression analysis, Student's t, and Pearson correlation tests. RESULTS: MPV was significantly higher and the mean platelet counts were significantly lower in diabetics compared to age- and sex-matched nondiabetic healthy controls [10.62+/-1.71 fl vs. 9.15+/-0.86 fl (P=.00), 260.38+/-68.65 x 10(9)/l vs. 292.33+/-79.19 x 10(9)/l (P=.001)], respectively. CONCLUSIONS: Our results show significantly higher MPV in diabetic patients than in the nondiabetic controls. This suggests that platelets may play a role in the micro- and macrovascular complications of diabetic patients.     

The effect of cisapride on gallbladder contractility in type II diabetic patients.

BACKGROUND/AIMS: To investigate whether diabetics have altered gallbladder motility, and whether cisapride has any effect on gallbladder motility in these patients. The factors associated with abnormal gallbladder contractility, and with the effects of cisapride on gallbladder contractility in diabetics were also evaluated. METHODOLOGY: The gallbladder contractility parameters of 20 diabetics and 20 controls were assessed by real time ultrasonography. The same measurements were made after cisapride treatment in diabetics. RESULTS: Fasting gallbladder volume and residual gallbladder volume were statistically higher in the diabetic group than in the controls (P = 0.018 and P = 0.022, respectively). Multivariate analysis also showed a significant association between fasting gallbladder volume and existing diabetes (P = 0.0002). There was a significant positive correlation between level of hemoglobin A1c and fasting gallbladder volume (r = 0.48, P = 0.031). Responders to cisapride treatment had significantly higher hemoglobin A1c levels than nonresponders (6.6 +/- 1.3 vs. 9.1 +/- 1.8, respectively; P = 0.004). Logistic multiple regression analysis revealed that hemoglobin A1c level was the only independent factor that was predictive for efficacy of cisapride treatment. CONCLUSIONS: This study demonstrates that diabetics have impaired gallbladder contractility, and that control of diabetes is predictive for gallbladder contractility and response to cisapride therapy in these patients.     

Sodium-proton exchanges and platelet procoagulant activity in type 1 diabetic patients

Platelet sodium-proton exchange rate and phospholipid dependent procoagulant activity were measured in 31 type 1 diabetics (mean age 32.3 +/- 10.1 years) and 35 healthy subjects (mean age 35.4 +/- 9.4 years). The activity of platelet Na+/H+ exchanger was measured in platelet rich plasma, using an optical swelling assay, according to Rosskopf et al. Platelet procoagulant activity was measured in platelet rich plasma, platelet poor plasma and platelet/microparticles filtrated plasma, using Russell's viper venom (according to Jy and Horstman) and calibrated with ship L-alpha-phosphatidylethanolamine. We found that Na+/H+ exchange rate was significantly higher in diabetic patients in comparison to the controls (p = 0.0009). There was also a positive correlation between the activity of Na+/H+ exchanger and phospholipid dependent procoagulant activity in all plasma fractions. We did not find a significant association between Na+/H+ exchanger activity and metabolic parameters studied, however in patients with HbA1c level > 7.5% higher Na+/H+ exchange rates were noted. Total procoagulant activity did not rise significantly in diabetic patients, but was markedly higher in platelet poor and platelet filtrated plasma. It was supposed that it originated from platelet derived microparticles, enriched in phospholipids. Our results suggest that an increased platelet Na+/H+ exchange rate and raised procoagulant activity connected with platelet microparticles may enhance the risk of vascular damage in type 1 diabetic patients.     

Relationship between autonomic neuropathy and thermogenesis in non diabetic and diabetic obese patients

Autonomic neuropathy is a well known complication of diabetes. Diabetes is often superimposed on obesity. A reduction in the variability of the heart rate in the resting state has been demonstrated in 16 obese diabetic subjects as well as in 34 obese non-diabetic subjects. The coefficient of variation (CV) of the heart rate during 30 minutes of resting was significantly decreased in both obese groups (3.9 +/- 0.2% for the diabetics; 5.2 +/- 0.2%, p less than 0.01 for the non diabetics) as compared to their own controls (4.5 +/- 0.6% and 6.5 +/- 0.4%, respectively). Age also contributes to decreased heart rate variability. Furthermore, this defect of autonomic function has been correlated with the blunted glucose-induced thermogenesis (GIT) seen in both obese groups (r = 0.52, p. less than 0.001): the increase in energy expenditure over basal values following a 100 g oral glucose load was only 4.8 +/- 0.8% for the diabetic obese group (p less than 0.001), and 8.5 +/- 0.7% for the non-diabetic obese group (p less than 0.001) as opposed to their own controls (12.4 +/- 1.3% and 13.3 +/- 0.6% respectively). Measurement of the variability of heart rate in obese individuals may be of predictive value in assessing blunted glucose-induced thermogenesis in non diabetic and diabetic obese patients.     

Left ventricular function in well-controlled insulin-dependent (type I) diabetics--an echophonocardiographic study

A high prevalence of left ventricular dysfunction in insulin-dependent (type-I) diabetics has been reported. However, the exact influence of metabolic control and/or the coexistence of early diabetic microangiopathy is unknown. Thus, we assessed left ventricular function by echophonocardiography in 50 type-I diabetics (mean age 26 +/- 7.9 years), who showed a fairly good metabolic long-term control (mean hemoglobin A1: 8.8%) after the introduction to intensified insulin therapy in comparison with 50 age- and sex-matched controls. Type-I diabetics did not differ from controls in their left ventricular internal diameters, mean wall thickness, ratio of pre-ejection period to left ventricular ejection time and systolic shortening fraction. Isovolumetric relaxation period reflecting an early diastolic event was slightly but significantly prolonged in diabetic subjects, independent of metabolic control status or existence of early microangiopathy. Isovolumetric relaxation period showed a statistically significant correlation to age in type-I diabetics, but not in controls. Possibly, the diabetic status--although well-controlled, but not normalized--may biochemically alter the myocardium and might influence its diastolic properties.     

Angiotensin-converting enzyme (ACE): relationship to insulin-dependent diabetes and microangiopathy

Angiotensin-converting enzyme (ACE) is secreted by the vascular endothelium and serum activity may reflect endothelial damage. A study of 48 insulin-dependent diabetics, 15 with and 33 without evidence of diabetic retinopathy and 41 non-diabetic controls was performed. ACE activity was significantly elevated in the diabetics compared with controls (mean +/- SD 46 +/- 14 vs 35 +/- 9 U/l, p less than 0.001) (units in micromoles substrate converted/min/l serum). This elevation was more marked in diabetics with such evidence of microangiopathy as retinopathy or raised albumin excretion rate (AER) (51 +/- 14 U/l, p less than 0.0001), and also in those with raised AER alone (47.2 +/- 15 U/l, p less than 0.002). Patients with both raised AER and retinopathy had significantly higher ACE activities than those with no complications (53 +/- 15 vs 41.2 +/- 15 U/l, p less than 0.05). No correlation was found with glycosylated haemoglobin or smoking habits. We conclude that mean serum angiotensin converting enzyme activity is increased in insulin-dependent diabetes, particularly in those with evidence of microangiopathy and this may reflect microvascular damage.     

Effect of a three-amino acid deletion in the alpha2B-adrenergic receptor gene on long-term body weight change in Finnish non-diabetic and type 2 diabetic subjects.

BACKGROUND AND OBJECTIVE: The short form (Glu9/Glu9) of the 12Glu9 deletion polymorphism of the alpha2B-adrenergic receptor gene was previously found to be associated with reduced basal metabolic rate in obese subjects. We investigated the effects of this polymorphism on changes in body weight in Finnish non-diabetic and type 2 diabetic subjects during a 10 y follow-up. DESIGN: Controlled 10 y follow-up study with baseline, 5 and 10 y examinations. SUBJECTS: A total of 126 non-diabetic control subjects and 84 newly diagnosed, middle-aged type 2 diabetic patients from eastern Finland participated. MEASUREMENTS: Anthropometric measurements, blood pressure, oral glucose tolerance test, plasma insulin, plasma C-peptide and glycosylated hemoglobin A1c. Genotypes were determined by polymerase chain reaction followed by agarose gel electrophoresis. RESULTS: No significant differences were found in the prevalence of the 12Glu9 deletion polymorphism between non-diabetic and type 2 diabetic subjects. The non-diabetic subjects with the Glu9/Glu9 genotype had a greater increase in their mean body weight during 5 y follow-up than the non-diabetic subjects with other genotypes (changes in body weight 0.4+/-5.7, -0.5+/-6.4 and 3.4+/-4.9% for the Glu12/Glu12, Glu12/Glu9 and Glu9/Glu9 genotypes, respectively, P=0.040 for the difference between the groups). Also, the trend for the increment of body weight was statistically significant in the non-diabetic subjects with the Glu9/Glu9 genotype (P=0.012). The 12Glu9 polymorphism was not cross-sectionally or longitudinally associated with body weight in type 2 diabetic subjects. CONCLUSIONS: The genotype of two short alleles (Glu9/Glu9) was associated with an increase in body weight among non-diabetic subjects.     

Sulfonylurea-induced decrease of muscle capillary basement membrane thickness in diabetes

Three muscle biopsies were performed in 53 overt type 2 diabetics over a period of approximately 2 years. At baseline, 21 (40%) had an increased capillary basement membrane width in muscle. Thirty-five patients received glipizide and 18 received placebo. In the patients receiving placebo, the mean of the muscle capillary basement membrane width increased from 158.7 +/- 11.5 nm (SEM) to 170.9 +/- 14.7 nm (P = NS), but in those receiving glipizide the value decreased from 192.9 +/- 13.2 nm to 161.0 +/- 10.2 nm (P = 0.02). Plasma glucose and glycosylated hemoglobin A1 decreased significantly (P less than 0.001) after 2 years in patients receiving glipizide. In 15, mean glycosylated hemoglobin A1 reached a normal range, and mean basement membrane width decreased to a level close to that found in subjects without diabetes (P = NS). These findings are consistent with the hypothesis that effective response to oral medication can decrease the basement membrane thickening, suggesting that diabetic microangiopathy is not necessarily progressive.     

Glycosylated hemoglobin in patients with newly discovered juvenile-onset diabetes mellitus in the days immediately following the beginning of insulin treatment

Summary We studied the behavior of fast hemoglobin fractions in newly discovered diabetic patients, before and in the 10 days immediately following the beginning of insulin therapy, in order to verify whether or not the rapid improvement of glycemic control involved a rapid reduction of total HbA₁ and of its fractions. We observed a rapid and highly significant fall of HbA_1(a+b+c) and HbA_1c levels after only 1 or 2 days of insulin therapy, followed by a slower decrement in the other 3–10 days. HbA_1(a+b) showed a slower decrement trend, reaching levels significantly below baseline values only after 7–10 days. These results suggest that rapid changes occurring in glycosylated hemoglobin levels after the beginning of insulin treatment in newly discovered diabetic patients involve mainly HbA_1c. The kinetics of glycosylated hemoglobin reduction, with a first rapid decrement followed by a slower one, may suggest the hypothesis that rapid changes are due to reversible Schiff base de-glycosylation, the ketoamine linkage being the true index of long term glycemic control.     

Non-enzymatic glycation of apolipoprotein B in the sera of diabetic and non-diabetic subjects.

Utilising a combination of m-aminophenyl-borate affinity chromatography and an immunoradiometric assay for apolipoprotein B (apo B), we have developed a specific and highly sensitive (6 ng/ml) procedure for the assay of glycated apo B. We studied 52 diabetic patients, 50 non-diabetic control subjects and 12 patients heterozygous for familial hypercholesterolaemia (FH). Both insulin-dependent and non-insulin dependent diabetics were included in our study. Total apo B in the diabetics (108 +/- 5 mg/dl; mean +/- S.E.M) was increased (controls: 95 +/- 4 mg/dl; P less than 0.05). In the FH group the serum apo B concentration (216 +/- 24 mg/dl) was significantly higher (P less than 0.001) than both the other groups studied. Both the serum glycated apo B concentration (9.3 +/- 0.8 mg/dl versus 4.8 +/- 0.7 mg/dl) and the percentage glycated apo B (7.9 +/- 0.4% compared to 3.9 +/- 0.2%) were significantly higher in the diabetics than in non-diabetic controls (P less than 0.001). A positive correlation was found between the percentage of glycated apo B and glycated haemoglobin (r = 0.65; P less than 0.001) and fasting glucose concentration (r = 0.52; P less than 0.001) in diabetics. The percentage of glycated apo B in FH patients was not significantly different from controls, but the serum concentration of glycated apo B, because of the greatly increased total level of apo B was raised (8.2 +/- 1.4 mg/dl) to a similar extent to that of the diabetics.     

Arterial wall compliance in diabetes.

A non-invasive Doppler ultrasound technique, based on the measurement of pulse wave velocity along the aorta, has been used to deduce aortic compliance in 25 Type 1 and 25 Type 2 diabetic patients. Thirteen of the Type 1 diabetic group had their compliance measured within 1 year of diabetes first being clinically diagnosed. All compliance values were normalized for age and sex variations using data previously obtained from over 600 normal, non-diabetic subjects (mean normalized compliance +/- SD; 100 +/- 15%). The results show that Type 1 diabetic patients have significantly more distensible aortas (132 +/- 26%) than their age- and sex-matched non-diabetic counterparts (100 +/- 12%) (p less than 0.01), while Type 2 diabetic patients have significantly stiffer aortas (74 +/- 21%) than their age- and sex-matched non-diabetic counterparts (100 +/- 18%) (p less than 0.01). The young Type 1 diabetic patients measured within 1 year of diagnosis have aortas ranging up to 78% more distensible (151 +/- 15%) than their age- and sex-matched non-diabetic controls (100 +/- 11%) (p less than 0.001). These results support findings by other groups that adult diabetic patients have less distensible arteries than normal, but contradict reports in the literature dating back over 20 years that diabetic children have stiffer arteries than normal children.