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Biomedical subjects

R B Tattersall

Publications and source records attributed to R B Tattersall.

At least 55 records · Page 3Linked to original sources
PubMed1990

Beta-adrenoceptor blockade and hypoglycaemia. A randomised, double-blind, placebo controlled comparison of metoprolol CR, atenolol and propranolol LA in normal subjects.

1. The effect of 1 week of treatment with propranolol LA (160 mg), atenolol (100 mg) and metoprolol CR (100 mg) on awareness of and the physiological responses to moderate hypoglycaemia were compared with placebo using a randomised, cross-over design in 12 healthy volunteers. 2. All three beta-adrenoceptor antagonists reduced resting heart rate, systolic blood pressure and heart rate responses to submaximal exercise compared with placebo. 3. Under hyperinsulinaemic (60 mu m-2 min-1) clamp conditions, at a blood glucose of 2.5 mmol l-1, atenolol prevented the rise in systolic and atenolol and metoprolol CR prevented the fall in diastolic blood pressure usually associated with hypoglycaemia. At this level of hypoglycaemia, the expected increase in heart rate was inhibited by atenolol but not metoprolol CR. Pre-treatment with propranolol LA resulted in a significant pressor response and a bradycardia during hypoglycaemia. In addition the normal increase in finger tremor was abolished by propranolol LA. 4. During hypoglycaemia all three beta-adrenoceptor blockers augmented sweating compared with placebo but hypoglycaemic symptoms, awareness and slowing of reaction time were the same with drugs and placebo. 5. The rise in plasma adrenaline and other counter-regulatory hormones during hypoglycaemia was enhanced by beta-adrenoceptor blockade. 6. We conclude that beta-adrenoceptor antagonists modify the physiological and hormonal responses to, but do not adversely affect awareness of, moderate hypoglycaemia in healthy volunteers.

Adrenergic beta-Antagonists↗
PubMed1989

Human insulin.

Explore the source record for details and available documents.

Animals↗
PubMed1989

Adaptation to mild hypoglycaemia in normal subjects despite sustained increases in counter-regulatory hormones.

In diabetes, loss of awareness of and a defective hormonal response to hypoglycaemia have been associated with long disease duration, improved glycaemic control and possibly a change in insulin species. In contrast it is assumed that normal subjects always have symptoms when their blood glucose is low. We have tested this in 7 normal subjects at 3 levels of blood glucose (4.5, 3.5 and 3.0 mmol/l) using a hyperinsulinaemic glucose clamp with a euglycaemic (4.5 mmol/l) clamp as a control. After 60 min at a blood glucose of 3.5 mmol/l adrenaline and glucagon increased slightly but significantly, whereas cortisol, growth hormone and pancreatic polypeptide were unchanged. As soon as glucose was lowered to 3.0 mmol/l adrenaline increased to 1.10 nmol/l and rose further to 1.43 nmol/l after 60 min. Glucagon secretion increased similarly but other counter-regulatory hormones were significantly raised only after 60 min at 3.0 mmol/l. Awareness of hypoglycaemia (symptom score) increased after 40 min at a blood glucose of 3.0 mmol/l but after 60 min decreased to baseline levels with loss of awareness in 5 subjects. Reaction time improved in parallel with the change in symptom score. Thus, despite high levels of adrenaline, normal subjects lose awareness during sustained mild hypoglycaemia. Improved reaction time may reflect cerebral adaptation.

Acclimatization↗
PubMed1989

Influence of duration of hypoglycemia on the hormonal counterregulatory response in normal subjects.

Glucagon and epinephrine are the most important short term glucose counterregulatory hormones. The epinephrine response in patients with insulin-dependent diabetes mellitus is related to the level of glycemic control, but little is known about the factors influencing counterregulation in normal subjects. We, therefore, conducted hyperinsulinemic glucose clamp studies to examine the counterregulatory response to recurrent and prolonged mild hypoglycemia in normal women. Blood glucose was clamped for 20 min at 3.5 mmol/L. Thereafter, the subjects had their blood glucose maintained at 2.8 mmol/L for 90 min and on another occasion lowered to 2.8 mmol/L and raised to 3.5 mmol/L twice during the 90-min period. Continuous hypoglycemia produced augmented plasma glucagon, cortisol, and pancreatic polypeptide responses (all P less than 0.05) compared to these responses to recurrent hypoglycemia. Plasma GH increased, but the magnitude of the response was not altered by the duration of hypoglycemia. During the recurrent hypoglycemia study plasma epinephrine levels rose and fell in parallel with the fluctuations in blood glucose. The mean peak increase was similar [1.37 +/- 0.25 (+/- SE) nmol/L] to that during the continuous study (1.76 +/- 0.23 nmol/L). There was no change in plasma glucagon levels in response to hypoglycemia of less than 15-min duration. We conclude that 1) the duration of hypoglycemia influences the counterregulatory response, and 2) epinephrine release is under precise control and responds rapidly to fluctuations in blood glucose.

Adult↗
PubMed1988

Comparison of high fibre diets, basal insulin supplements, and flexible insulin treatment for non-insulin dependent (type II) diabetics poorly controlled with sulphonylureas.

OBJECTIVE: To compare high fibre diet, basal insulin supplements and a regimen of insulin four times daily in non-insulin dependent (type II) diabetic patients who were poorly controlled with sulphonylureas. DESIGN: Run in period lasting 2-3 months during which self monitoring of glucose concentration was taught, followed by six months on a high fibre diet, followed by six months' treatment with insulin in those patients who did not respond to the high fibre diet. SETTING: Teaching hospital diabetic clinics. PATIENTS: 33 patients who had had diabetes for at least two years and had haemoglobin A1 concentrations over 10% despite receiving nearly maximum doses of oral hypoglycaemic agents. No absolute indications for treatment with insulin. INTERVENTIONS: During the high fibre diet daily fibre intake was increased by a mean of 16 g (95% confidence interval 12 to 20 g.) Twenty five patients were then started on once daily insulin. After three months 14 patients were started on four injections of insulin daily. ENDPOINT: Control of diabetes (haemoglobin A1 concentration less than or equal to 10% and fasting plasma glucose concentration less than or equal to 6 mmol/l) or completion of six months on insulin treatment. MEASUREMENTS AND MAIN RESULTS: No change in weight, diet, or concentrations of fasting glucose or haemoglobin A1 occurred during run in period. During high fibre diet there were no changes in haemoglobin A1 concentrations, but mean fasting glucose concentrations rose by 1.7 mmol/l (95% confidence interval 0.9 to 2.5, p less than 0.01). With once daily insulin mean concentrations of fasting plasma glucose fell from 12.6 to 7.6 mmol/l (p less than 0.001) and haemoglobin A1 from 14.6% to 11.2% (p less than 0.001). With insulin four times daily concentrations of haemoglobin A1 fell from 11.5% to 9.6% (p less than 0.02). Lipid concentrations were unchanged by high fibre diet. In patients receiving insulin the mean cholesterol concentrations fell from 7.1 to 6.4 mmol/l (p less than 0.0001), high density lipoprotein concentrations rose from 1.1 to 1.29 mmol/l (p less than 0.01), and triglyceride concentrations fell from 2.67 to 1.86 mmol/l (p less than 0.05). Patients taking insulin gained weight and those taking it four times daily gained an average of 4.2 kg. CONCLUSIONS: High fibre diets worsen control of diabetes in patients who are poorly controlled with oral hypoglycaemic agents. Maximum improvements in control of diabetes were achieved by taking insulin four times daily.

Blood Glucose↗
PubMed1988

Alpha glucosidase inhibition in the treatment of non-insulin-dependent diabetes mellitus.

Two studies of the new alpha-glucosidase inhibitor, miglitol, in patients with non-insulin-dependent diabetes mellitus (NIDDM) are reported. In the first, 13 patients, poorly controlled on sulphonylureas, received miglitol 50mg three times daily for 4 weeks. Post-prandial blood glucose was reduced after breakfast, lunch, and tea compared with placebo (p less than 0.05-0.01) but there was no improvement in fasting blood glucose, serum fructosamine or haemoglobin A1. In a dose-response study the effect of a single dose of miglitol (0,50,100,150 or 200mg) on post-prandial glycaemia after a test breakfast was assessed in 20 patients with mean +/- SEM fasting blood glucose 9.9 +/- 0.4 mmol/l. With 50mg miglitol, there was a significant reduction in blood glucose from 30 to 120 min post-prandially compared with placebo. Increasing doses of miglitol further depressed the post-prandial rise in blood glucose and with 200mg there was no significant change from fasting levels. Side-effects were limited to flatus and loose stools particularly with the higher doses but were not severe. Miglitol effectively reduces post-prandial blood glucose rise in NIDDM with as little as 50mg but there is considerable individual variation. Larger doses may be necessary in patients already poorly controlled on sulphonylureas.

1-Deoxynojirimycin↗
PubMed1988

Group education for obese patients with type 2 diabetes: greater success at less cost.

It has been suggested that much effort expended in teaching diabetic diets is ineffective and wasteful. We have tested a different system by randomly allocating 75 newly diagnosed obese Type 2 diabetic patients to usual 'unstructured' clinic care or to group education by diabetes specialist nurses and a dietitian. Patients allocated to group education attended five 90-min group sessions during the first 6 months. Six months after diagnosis they had lost more weight (median (95% Cl), 7 (5.5-9) vs 2(1-5)kg, p less than 0.002) and were better controlled (HbA1:7.5 (7.0-8.1) vs 9.5 (8.7-10.4)%, p less than 0.001) than those randomized to the usual clinic system. At 1 year (after no further visits) the difference in weight loss was less (5.5 (4-6.5) vs 3 (2-4) kg, p less than 0.05) and diabetic control was similar (HbA1:9.0(8.2-9.8) vs 9.9(8.9-10.9)%. At 1 year only 14(39%) of the education group and 9(23%) of those attending the clinic had a fasting blood glucose less than 7.0 mmol l-1.

Blood Glucose↗
PubMed1988

Abnormal thermoregulation in diabetic autonomic neuropathy.

Hypothermia has been reported to be more common in diabetic people than in nondiabetic people, and we have investigated the possibility that autonomic neuropathy may be associated with disordered thermoregulation. After an overnight fast and maintenance of normoglycemia, 12 insulin-treated diabetic patients with and 11 without neuropathy and 12 nondiabetic control subjects, all less than 55 yr, were subjected to external cooling by perfusing water at 16 degrees C through a liquid-conditioned coverall for less than or equal to 45 min. Patients with autonomic neuropathy had impaired vasoconstriction to cooling, particularly in the foot, calf, and forearm. Core temperature rose by 0.2 degrees C in control subjects and by 0.15 degrees C in patients with diabetes but no neuropathy. In contrast, group mean core temperature was unchanged in those with autonomic neuropathy and fell in 3 subjects (P less than .001). Cooling caused shivering in 6 patients with diabetic autonomic neuropathy, but not in those with neuropathy or control subjects (P less than .05). Baseline metabolic rates were similar in all three groups, but the increase after cooling was significantly greater among those who shivered (P less than .05-.02). Thus, young diabetic patients with autonomic neuropathy have impaired thermoregulation to a relatively short period of external cooling, even during metabolic stability, which may predispose to hypothermia.

Adult↗
PubMed1988

Censoring of patient-held records by doctors.

Computer-held information is increasingly shared between general practice and hospitals and with the provisions of the Data Protection Act now in operation, the practical issues of disclosure to patients need to be reviewed. Patients attending diabetic clinics at University Hospital, Nottingham, are routinely issued with a copy of their computerheld record but a previous study showed a high level of censoring by the hospital doctors. This paper reports a review of a sample of 251 censored records, containing 426 problems, whereby the doctors concerned provided reasons for the censoring and restored information they thought suitable. After the review, only 8% of censored problems, that is 1% of all problems, remained censored. An additional 2% of all problems were deleted from the patient's copy at the request of the patient. It is essential that systems which allow censoring of patient records have continuous built-in audit to monitor the reasons for censoring.

Computers↗
PubMed1987

Influence of sympathetic nervous system on hypoglycaemic warning symptoms.

The effect of mild insulin-induced hypoglycaemia on symptoms, physiological changes, and adrenaline responses was assessed in 10 normal subjects and 15 insulin-dependent diabetic patients (5 with reduced awareness of hypoglycaemic symptoms). When blood glucose was maintained at 3.2 mmol/l, reaction time was prolonged in both normal and diabetic subjects and plasma adrenaline levels increased in the normals and some diabetics; there were no other physiological responses. 2 normals and 1 diabetic were aware that their blood glucose was low. When blood glucose was maintained at 2.5 mmol/l for 30 min, 9/10 normals but only 4/15 diabetics recognised hypoglycaemia. Increases in hypoglycaemic symptom score, tremor, and sweating, and falls in diastolic blood pressure were significant only in the normal subjects and the 4 "aware" patients. Adrenaline levels increased in all cases, but were more pronounced in the normals and aware diabetics. Reaction time remained prolonged in all groups. All measurements returned to baseline when blood glucose was raised to 4.5 mmol/l. Impairments in adrenaline response may be common, even in diabetic patients without autonomic neuropathy and in those who do not complain of hypoglycaemic unawareness; consequent failure to recognise a falling blood glucose may predispose to a risk of severe hypoglycaemia.

Adult↗
PubMed1987

Causes of death in diabetic patients with impaired renal function. An audit of a hospital diabetic clinic population.

Of over 2000 diabetic patients whose serum creatinine had been measured regularly, 107 died between January, 1983, and March, 1985, and 27 (median age at death 66 years) had renal impairment (serum creatinine over 130 mumol/l). Cause of death was determined from clinical and necropsy data. 11 died of cardiovascular disease and 10 of causes unrelated to cardiac or renal disease; in only 6 was renal impairment the main cause of death. All 6 had severe physical and/or social disabilities and 2 were over the age of 75. Median serum creatinine in patients who died was 269 mumol/l (range 135-1135 mumol/l) and exceeded 500 mumol/l in only 5. Of the few patients who would have received RRT under a more liberal dialysis policy, all had severe physical disabilities.

Adult↗
PubMed1987

Counterregulation in type 2 (non-insulin-dependent) diabetes mellitus. Normal endocrine and glycaemic responses, up to ten years after diagnosis.

We have examined hormonal and metabolic responses to insulin-induced hypoglycaemia in 10 Type 2 (non-insulin-dependent) diabetic patients treated with tablets and 10 age, sex and weight matched control subjects. Diabetic patients were under 110% ideal body weight, had no autonomic neuropathy and were well controlled (HbA1, 7.1 +/- 0.2%). After the diabetic patients were kept euglycaemic by an overnight insulin infusion, hypoglycaemia was induced in both groups by intravenous insulin at 30 mU.m-2.min-1 for 60 min and counterregulatory responses measured for 150 min. There were no significant differences between diabetic patients and control subjects in the rate of fall (3.3 +/- 0.3 vs 4.0 +/- 0.3 mmol.l-1.h-1), nadir (2.4 +/- 0.2 vs 2.3 +/- 0.1 mmol/l) and rate of recovery (0.027 +/- 0.002 vs 0.030 +/- 0.003 mmol.l-1.min-1) of blood glucose. Increments of glucagon (60.5 +/- 5.7 vs 70 +/- 9.2 ng/l) and adrenaline (1.22 +/- 0.31 vs 1.45 +/- 0.31 nmol/l) were similar in both groups. When tested using this model, patients with Type 2 diabetes, without microvascular complications and taking oral hypoglycaemic agents show no impairment of the endocrine response and blood glucose recovery following hypoglycaemia.

Adult↗
PubMed1987

Serum C-peptide after 6 months on glibenclamide remains higher than during insulin treatment.

Serum C-peptide was measured fasting and 6 minutes after glucagon (1 mg given intravenously) in 49 patients with non-insulin-dependent diabetes mellitus, after 4 and 6 months of successive periods of treatment with insulin and oral hypoglycaemics (glibenclamide and metformin), given in random order. Glycaemic control was not significantly different on the two treatments, but C-peptide was much higher while the patients were on glibenclamide. We conclude that glibenclamide stimulates pancreatic insulin production even after 6 months treatment.

Adult↗
PubMed1986

Starting insulin treatment as an outpatient. Report of 100 consecutive patients followed up for at least one year.

Most textbooks advise that newly diagnosed insulin-dependent diabetics be admitted to the hospital. Nevertheless, if they are not acutely ill, we start insulin treatment on an outpatient basis. We report herein the logistics, efficacy, and safety of our system. Over two years, 115 newly diagnosed insulin-dependent diabetics were seen in our hospital. Fifteen (66% of them ketoacidotic) were admitted. The other 100 were treated as outpatients by a nurse specialist with a starting dosage of 6 to 10 units of intermediate-acting insulin twice daily. Hemoglobin A1 concentration at diagnosis was 15.2% +/- 2.7% (mean +/- SD); at six months, 10.9% +/- 2.9%; and at one year, 10.6% +/- 2.8%. Only three outpatient starters were hospitalized in the first year, one for hypoglycemia and two with respiratory tract infections. Our findings suggest that outpatient stabilization is both safe and cost-effective.

Adolescent↗
PubMed1985

A prospective comparison of 'conventional' and high carbohydrate/high fibre/low fat diets in adults with established type 1 (insulin-dependent) diabetes.

Diabetic associations throughout the world are recommending high carbohydrate/high fibre/low fat diets for diabetic patients as a means of improving general health and metabolic control. We have previously shown that the efficacy of a 'conventional' low carbohydrate diet can be greatly increased by improving the method of dietary education. To test whether further improvement in metabolic control could be achieved by changing to a high carbohydrate/high fibre/low fat diet we have followed a group of 40 Type 1 (insulin dependent) diabetic adults for up to 19 months. They had all been prescribed a conventional low carbohydrate diet taught by one of three methods (dietician only, practical lunchtime demonstration or videotape). Those taught by dietician only were left as a control group for follow-up (group A). The others were randomized either to continue on their present diet (group B) or to change to a high carbohydrate/high fibre/low fat diet (group C). At final assessment those in groups B and C were more knowledgeable, compliant and better controlled than group A. Those in group C achieved a change from 38% carbohydrate/43% fat/20 g fibre daily to 45% carbohydrate/34% fat/32 g fibre daily. However, metabolic control in group C deteriorated while taking the high carbohydrate/high fibre/low fat diet (haemoglobin A1 went from 9.4 +/- 0.5% to 11.2 +/- 0.5%, p less than 0.01, over 4 months). None of the patients in group C changed their eating habits or those of their families nearly as much as was recommended.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗