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Biomedical subjects

T D Hockaday

Publications and source records attributed to T D Hockaday.

At least 73 records · Page 4Linked to original sources
PubMed1985

Polyunsaturated fatty acids and diabetic retinopathy.

One hundred and forty nine diabetic patients were ophthalmologically assessed seven years after randomisation to a low carbohydrate or modified fat diet (rich in linoleic acid). Glycaemic control, regardless of the type of diet, was a major determinant of the development of retinopathy. Poorly controlled patients (haemoglobin A1c greater than 8%) with low levels of linoleic acid in cholesterol ester had a significantly greater frequency of retinopathy than well controlled patients or patients with similarly unsatisfactory control but higher levels of linoleic acid. The findings support an earlier suggestion that linoleic acid might protect against diabetic retinopathy.

Cholesterol Esters↗
PubMed1985

Blood pressure at diagnosis of type 2 diabetes correlates with plasma insulin concentration but not during the next 5 years.

At diagnosis of non-insulin-requiring diabetes, in 215 patients, systolic and diastolic (Korotkow 4) blood pressures, corrected for arm circumference, correlated with fasting plasma insulin concentration (r = 0.29, p less than 0.001), body mass index (BMI) (W/H2), and age (p less than 0.05 in all cases for both systolic and diastolic pressures). Women had higher pressures but were also heavier than men. Systolic pressure fell by 13 +/- SD 11%, diastolic by 8 +/- 15%, over 1 month and remained decreased over 5 yr. The fall was greater with high initial pressure (r = 0.6-0.7, p less than 0.001 all years). The correlation of initial pressure with plasma insulin remained significant even when allowing for age, surface area, BMI, and plasma concentrations of glucose, urea, creatinine, sodium and urate. Neither gender nor treatment with sulphonylureas or hypotensives influenced this relationship. During the first 5 yr after diagnosis the correlation between blood pressure and insulin weakened, particularly when allowing for the factors above (at 5 yr, systolic p = 0.025, diastolic NS).

Adult↗
PubMed1985

Mortal factors in type 2 (NIDDM) diabetes mellitus.

Five years after entry into a study prospective from diagnosis of non-insulin-dependent (Type 2) diabetes, 17 patients were known to be dead and 197 alive. On analysis of 136 patients (12 deaths) in whom there was complete information from clinical, metabolic and hormonal examination both before and 1 yr after start of treatment, an index of liability to death within this first 5 yr was calculated, to separate best the dead from the living. One index value correctly ascribed 83% of the dead and 90% of the living (89% of all predictions correct; Youden's "J" value = 0.73). Estimates from the less complete data on the other 78 patients (5 deaths) did not alter the predictive factors. Prediction is more successful with non-cardiac than with cardiac deaths. Five factors contributed to the predictive index for death. One was a long duration of symptoms as recalled at diagnosis. The other 4 factors all came from the 1-yr review (no death then). These were (a) greater glucose intolerance, as expressed by the KG rate constant for disappearance of i.v. injected glucose from the blood (more useful than fasting glucose concentration); (b) higher systolic blood pressure (more useful than diastolic); (c) less obesity, as expressed by the Body Mass Index, and (d) higher fasting blood glycerol concentration. As expected, hyper-glycaemia (as reflected in the KG value) is important, but adrenergic factors may contribute to (a), (b) and (d). From these results earlier diagnosis of this type of diabetes could well be associated with an improved outlook, and in addition this alone might ameliorate the other factors, but measures to normalise them post-diagnosis also require testing.

Blood Glucose↗
PubMed1984

Fasting plasma magnesium concentrations and glucose disposal in diabetes.

Fasting plasma concentrations of magnesium were measured by neutron activation analysis in 30 non-diabetics and 87 diabetics (55 non-insulin-treated, 32 insulin treated). Plasma concentrations of magnesium were lowest in the insulin treated group (mean 0.84 (SEM 0.01) mmol/1; 2.0 (0.02) mg/100 ml), intermediate in the non-diabetics (mean 0.89 (SEM 0.01) mmol/1; 2.2 (0.02) mg/100 ml), and highest in the non-insulin-treated diabetics (mean 0.95 (SEM 0.02) mmol/1; 2.3 (0.05) mg/100 ml). In all diabetics plasma magnesium concentrations were inversely related to plasma glucose values (rs = -0.33; p less than 0.01) and in non-insulin-treated patients to plasma insulin concentrations (rs = -0.28; p less than 0.05), the former confirming previous observations. In 67 of the diabetics the KG constant for disposal rate of glucose during a standard intravenous glucose tolerance test was directly related to fasting plasma magnesium concentrations, and this relation persisted after controlling for age, sex, body mass index, type of treatment, and glucose and insulin values. This direct relation of plasma magnesium concentration with glucose disposal was unexplained by its influence on insulin secretion but was related to insulin sensitivity; hence magnesium may be an important determinant of insulin sensitivity in maturity onset diabetes.

Blood Glucose↗
PubMed1984

Retinopathy is associated with higher glycaemia in maturity-onset type diabetes.

In a group of 149 maturity-onset type diabetic patients followed from diagnosis, 55 (37%) had retinopathy on colour photography 7 years later. Those patients with retinopathy had significantly greater glycaemia, as shown by higher fasting plasma glucose levels at diagnosis, larger mean values for fasting glucose 1, 3 and 5 years later, and higher random glucose and haemoglobin A1c at ophthalmic review (p = 0.001, 0.002, 0.007 and 0.001, respectively). Substantial retinopathy, as measured by greater than 5 microaneurysms, also correlated significantly with each index of glycaemic control.

Blood Glucose↗
PubMed1984

Urinary excretion of non-dialysable conjugates of glucose and galactose in normal people and diabetic patients.

Urine contains non-dialysable conjugates of glucose and galactose from which the free sugars are released by acid hydrolysis. In 14 non-diabetic subjects the 24-h outputs (mean +/- SEM) were 25 +/- 3 mumol/24 h (glucose) and 109 +/- 15 mumol/l (galactose). In collections from 23 diabetic patients output of conjugated glucose was increased to 177 +/- 96 mumol/24 h but conjugated galactose was unchanged (119 +/- 10 mumol/24 h). The concentration ratio of glucosyl/galactosyl allows relative 24-h outputs of conjugated glucose to be estimated on random samples. The ratio (mean +/- SEM) was 0.24 +/- 0.01 in 27 normal men and 0.37 +/- 0.04 in 30 normal women. The mean ratio was increased to 0.72 +/- 0.20 in 56 male and to 0.51 +/- 0.07 in 17 female diabetic patients. In individual diabetic patients, the ratio was increased significantly in 28 out of 56 men and in 5 out of 30 women. In male diabetic patients the ratio was increased in 17 out of 23 Type 1 (insulin-dependent) but in only 3 out of 15 Type 2 (non-insulin-dependent) diabetic patients. There was no correlation between the glucosyl/galactosyl ratio and patient age, known duration of diabetes, or urinary excretion of free glucose or protein. Urine samples showing increased glucosyl/galactosyl ratios did not yield bacteria on culture and were negative for Candida albicans cell-wall mannan antigen. It is concluded that 80% of male Type 1 diabetic patients show increased urinary excretion of non-dialysable conjugated glucose. In women, there is much greater variation in non-diabetic subjects which may obscure an increased excretion in diabetic patients.

Adult↗
PubMed1984

Hyperglycaemia is one correlate of deterioration in vibration sense during the 5 years after diagnosis of type 2 (non-insulin-dependent) diabetes.

Seventy-one Type 2 (non-insulin-dependent) diabetic patients showed only a slight deterioration in mean vibration sensory threshold (measured biothesiometrically) on the feet during the 5 years from diagnosis. However, multiple linear regression analysis of the wide range of individual changes in this threshold showed as significant independent associated factors the initial sensory threshold (p less than 0.001), age, gender, and both the mean fasting blood glucose and failure to become thinner under treatment (p less than 0.05 for all). The relationship with fasting glucose was stronger if the pre-treatment value was included in calculation of the mean (p less than 0.001). Mean fasting blood glucose under treatment accounted for only a small fraction of the total variance of the deterioration of the vibration sensory threshold, but represented one-twelfth of that attributable to identified factors, and one-third of the variance ascribable to factors subject to therapy. Interim values revealed the persistent effect of hyperglycaemia over the 5 years. An increase of 1 mmol/l in mean fasting blood glucose has an equivalent effect on the sensory threshold to an extra 5 years of age.

Age Factors↗
PubMed1984

Non-uniform distribution of islet amyloid in the pancreas of 'maturity-onset' diabetic patients.

Quantitative morphometry of the pancreases of five 'maturity-onset' diabetic subjects has demonstrated more amyloid in islets of the head, body and tail (where it was found in a mean 29% of the islets occupying a mean 11% islet area) than in islets of the 'pancreatic-polypeptide-rich' lobule of the head (where amyloid was found in a mean of 3% of the islets occupying a mean of 0.7% islet area, both p less than 0.005). The non-uniform amyloid distribution may relate to the hormone content of the islet; the head and tail contained significantly more A, B and D-cells than the pancreatic-polypeptide-rich lobule in both non-diabetic subjects (n = 8) and diabetic patients (n = 5; p less than 0.005). This result is compatible with the previous suggestion that amyloid may be derived from insulin or its precursors.

Aged↗
PubMed1984

Fatty acid composition of platelet phospholipids in non-insulin-dependent diabetics randomized for dietary advice.

Two groups of patients with non-insulin-dependent diabetes mellitus (NIDDM), with dietary advice randomized between a low-carbohydrate (LC) diet and a modified-fat (MF) diet, were followed to determine the effect of diet on phospholipid fatty acid composition of platelets and on development of retinopathy in the 7 years following diagnosis. There was a tendency for retinopathy to occur more frequently in those randomized to the LC diet. This difference was not statistically significant, and fatty acid composition of platelets did not differ significantly in those with and without retinopathy. Linoleic acid values from platelet phospholipid fatty acids were significantly higher in NIDDM on an MF diet compared with an LC diet. There was no difference between the two dietary subgroups with respect to platelet arachidonic acid, but this was lower in the whole diabetic population when compared with non-diabetics. The arachidonic acid values correlated with neither glycosylated haemoglobin nor mean glycaemia. Significant correlation between the fatty acid values for platelets and plasma cholesterol esters was found only for 16:0.

Blood Platelets↗
PubMed1984

A comparison of isocaloric high carbohydrate and high fat test meals in diabetics.

Ten diabetic patients were given test meals at breakfast and lunch on successive days to compare the acute glycaemic responses to meals either high (65%) (HC) or extremely low (12%) in carbohydrate; the latter was very high (71%) in fat (HF). The meals were isocaloric and fibre content, though higher in HC, was within the range of the average British intake for both diets. The mean fasting blood glucose levels were similar on the 2 days (9.8 mmol/l; 9.6 mmol/l) but mean peak post-prandial levels were significantly greater after the HC meals (17.7 mmol/l after breakfast and 14.1 mmol/l after lunch) than after the HF meals (11.7 mmol/litre after breakfast; P less than 0.02; 8.1 mmol/l after lunch; P less than 0.02). Mean blood glucose value for the 6-hr study period was significantly higher after the HC meals (14.0 mmol/l) than after the HF meals (9.2 mmol/l; P less than 0.001). There was no significant difference in mean fasting, peak or total mean triglyceride level. In the short term, therefore, meals very low in carbohydrate and high in fat are followed by a lower glycaemic response than meals high in carbohydrate but with only a usual (22 g/day) fibre content. Delayed gastric emptying after HF meals may well contribute to the results but long-term use of such HF meals is not advised in view of the extremely high fat content.

Blood Glucose↗
PubMed1984

Hyperinsulinaemia is associated with development of electrocardiographic abnormalities in diabetics.

Twelve-lead electrocardiograms (ECGs) were recorded at diagnosis from 247 initially non-insulin-requiring diabetics. The record was normal in 208 (84%) patients and abnormal in 39 (16%). The latter were older (p = 0.002), with higher blood pressures (diastolic and systolic) and greater cardiothoracic ratios (all p less than 0.02). They also had higher fasting (p less than 0.01) and post-glucose (p less than 0.04) plasma insulin concentrations per body mass index than those with normal ECGs. Five years later 17 patients had died (4 from proven and 6 from suspected cardiac cause), 5 had sustained a proven myocardial infarct and 3 a suspected cardiac event. ECGs were recorded from 138 patients both at diagnosis and 5 yr later. The record was normal on both occasions in 100 (72%), changed from normal to abnormal in 21 (15%), from abnormal to normal in 9 (7%), and was abnormal on both occasions in 8 (6%). Patients who developed ECG abnormalities were older (p = 0.011), and had greater mean fasting cholesterol during the 5 yr (p = 0.05). They also had greater fasting insulin levels per body mass index both before (mean of initial and 1-yr values, p = 0.02) and after the abnormality developed (p = 0.003) than those with persistently normal recordings. Insulin levels post-glucose were greater at 5 yr in those with cardiac abnormality but, as with the higher diastolic blood pressure and fasting glucose concentration then (both p less than 0.05), this difference was not significant initially. (ABSTRACT TRUNCATED AT 250 WORDS)

Diabetes Mellitus, Type 2↗
PubMed1983

Acute respiratory distress in diabetic ketoacidosis: possible contribution of low colloid osmotic pressure.

The "shock lung" syndrome may occur in diabetic ketoacidosis in association with disseminated intravascular coagulation; occasionally it occurs alone after treatment of the ketoacidosis. Two patients developed pulmonary opacities with clinical features of acute respiratory distress such as are seen in the shock lung syndrome; in both, however, the findings suggested a different mechanism from that occurring in the syndrome. Hypoalbuminaemia was prominent, and it is postulated that a low plasma osmotic pressure caused by high volume crystalloid infusions may have precipitated the acute respiratory complications. Plasma osmotic pressure may be an important variable in patients given large volumes of crystalloid infusions; further studies are required to elucidate mechanisms of pulmonary oedema in such patients.

Adult↗
PubMed1983

Chlorpropamide-alcohol flushing and plasma chlorpropamide concentrations in diabetic patients on maintenance chlorpropamide therapy.

Forty-three diabetic patients on maintenance chlorpropamide (100-750 mg daily) drank 0.2 ml/kg 90% ethanol after equilibration in a room controlled at 20 degrees C. Twenty-five patients had already noted marked alcohol flushing since starting chlorpropamide therapy (group A), while 13 had not observed this (group B). The remainder were teetotal or unsure of their reaction. Cheek temperature rise correlated with plasma chlorpropamide concentration (r = 0.6, p less than 0.001) in all patients and was inversely related to basal cheek temperature (r = -0.35, p less than 0.02). Plasma chlorpropamide correlated with daily chlorpropamide dose (r = 0.8, p less than 0.001) but not with basal cheek temperature. The correlation between chlorpropamide level and cheek temperature rise was strengthened on analysis of group A alone (r = 0.7, p less than 0.001) and absent in group B (r = 0.2, p greater than 0.3) who tended to have lower chlorpropamide levels and cheek temperature rise than group A.

Body Temperature↗