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Biomedical subjects

M Nattrass

Publications and source records attributed to M Nattrass.

At least 109 records · Page 6Linked to original sources
PubMed1982

Value of serum glucose assay as part of the biochemical profile in screening for diabetes.

The value of adding serum glucose assay to the 'biochemical profile' was assessed by a detailed follow-up of all inpatients with serum glucose concentrations of 10 mmol/l or more. After excluding patients who were on intravenous glucose infusions or were known to be diabetic. 1 in 10 was found to have unsuspected diabetes by further blood glucose measurements, glucose tolerance tests, and clinical assessment. The incidence was 0.8% of all inpatients receiving a biochemical profile, and in a full year 64 diabetics would be detected. The extra cost of laboratory tests was only 20 pounds for each diabetic detected.

Autoanalysis↗
PubMed1981

Effects of mild hyperinsulinemia on the metabolic response to exercise.

To assess the effects of mild hyperinsulinemia on the metabolic adaptations to exercise, five normal male subjects were studied during 2 cycles of 30 min rest followed by 60 min mild exercise. During one cycle, insulin was infused at a rate of 0.33 mU/kg/min. During both cycles, plasma glucose concentration was kept constant by a glucose-controlled glucose infusion system. Studies with and without insulin were performed in random order, with 30 min between studies. During the insulin infusion, plasma non-esterified fatty acids fell during rest and failed to rise with exercise, indicating a limited availability of this substrate to working muscle. Insulin infusion also inhibited the expected rise in glycerol and 3-hydroxybutyrate normally observed during exercise. Plasma lactate concentrations at the completion of exercise with insulin infusion were higher than after exercise without insulin infusion. Greater metabolic dependence on carbohydrate metabolism is suggested by an increased respiratory quotient during insulin infusion. Insulin infusion had no significant effect on the amount of glucose which needed to be infused for maintaining a constant plasma glucose during rest, but there was a large and significant difference in the need for infused glucose during exercise with and without insulin infusion. The results indicate that even mild hyperinsulinism interferes with normal metabolic responses to exercise, and suggest that fall in insulin concentration seen with exercise is an important regulatory process, not merely a secondary consequences of a declining plasma glucose level.

3-Hydroxybutyric Acid↗
PubMed1980

Hormonal and metabolic rhythms in Cushing's syndrome.

Hormone and metabolite profiles were investigated over a 12-hr period in six patients with Cushing's syndrome, ten age- and sex-matched normal controls, and six moderately obese subjects matched for weight with the patient group. Mean diurnal plasma cortisol levels were 563 +/- 74 nmole/liter in the patients, 275 +/- 22 nmole/liter in normal controls and 241 +/- 32 nmole/liter in obese subjects, with total loss of diurnal changes in Cushing's syndrome. Fasting blood glucose concentration was similar in all groups although mild hyperglycemia occurred after meals in the Cushing's patients compared with normal and obese subjects (mean 12-hr blood glucose: Cushing's 6.31 +/- 0.39 mmole/liter; normal controls, 5.32 +/- 0.14 mmole/liter, p < 0.01; obese subjects, 5.41 +/- 0.18 mmole/liter, p < 0.05) despite marked hyperinsulinemia (mean 12-hr serum insulin: Cushing's 57.3 +/- 18.2 mU/liter; normal controls, 19.7 +/- 2.5 mU/liter, p < 0.02; obese subjects, 18.1 +/- 4.0 mU/liter, p < 0.05). Concentrations of the gluconeogenic precursors lactate, pyruvate, and alanine were raised in Cushing's syndrome, particularly postprandially. Plasma nonesterified fatty acids (NEFA), blood glycerol, and blood ketone body concentrations were comparable in all three groups although the normal diurnal variation in circulating NEFA and ketone body levels was lost in Cushing's syndrome. Serum triglyceride (TG) concentrations were grossly elevated in the Cushing's patients (mean 12-hr serum TG: Cushing's 3.51 +/- 1.23 mmole/liter; normal controls 0.89 +/- 0.19 mmole/liter, p < 0.02; obese subjects, 0.93 +/- 0.23 mmole/liter, p < 0.05) and correlated positively with serum insulin levels. Plasma glucagon concentrations were raised in Cushing's syndrome (mean 12-hr plasma glucagon: Cushing's 23.2 +/- 3.7 pmole/liter; normal controls 12.3 +/- 1.5 pmole/liter p < 0.01; obese subjects 12.2 +/0 2.0 pmole/liter, p < 0.02) and correlated positively with the serum cortisol but not with blood alanine, suggesting that some stimulatory factor other than alanine was responsible. The metabolic effects of chronic glucocorticoid excess thus may not be explained on the basis of obesity alone. Compensatory hyperinsulinemia limits the disturbance of carbohydrate and lipid metabolism in Cushing's syndrome but may be important in production of the hypertriglyceridemia observed.

Adolescent↗
PubMed1980

Correlation of plasma phenformin concentration with metabolic effects in normal subjects.

1. Circulating concentrations of intermediary metabolites have been measured after administration of 50 mg of phenformin to normal subjects. 2. Phenformin caused a significant increase in blood lactate, alanine and the lactate/pyruvate ratio but did not affect blood glucose or serum insulin concentrations. 3. There was a significant correlation between the increase in blood lactate concentration after phenformin and the plasma concentration of the drug.

Adult↗
PubMed1980

Hyperinsulinaemia in hyperprolactinaemic women.

The metabolic sequelae of hyperprolactinaemia were studied over a 12 h period of normal meals and activity in nine young females hyperprolactinaemic subjects and fourteen matched controls. In the patients, fasting blood glucose and serum insulin concentrations were normal, as was the blood glucose response to meals; the insulin rise with meals was, however, exaggerated and hyperinsulinaemia persisted throughout the day (mean +/- SEM 12 h serum insulin, 26 +/- 8 vs. 16 +/- 9 mu/l, P < 0.01). Blood lactate, pyruvate and alanine response to meals was also increased. Blood glycerol (mean 12 h blood glycerol 0.06 +/- 0.01 vs. 0.09 +/- 0.01 mmol/l, P < 0.01) and blood 3-hydroxybutyrate (mean 12 h blood 3-hydroxybutyrate 0.03 +/- 0.01 vs. 0.05 +/- 0.01 mmol/l, P < 0.05) concentrations were lower in hyperprolactinaemic subjects. There was a strong negative correlation between mean insulin and mean 3-hydroxybutyrate levels in the afternoon period (rs = -0.92, P < 0.01). Excess circulating prolactin in young female is associated with normoglycaemic hyperinsulinaemia. The changes in blood metabolite levels observed are probably secondary to the increased insulin concentrations.

Adult↗
PubMed1979

Metabolic effects of combined sulphonylurea and metformin therapy in maturity-onset diabetice.

Twelve hour metabolic studies have been performed in two groups of maturity-onset diabetics treated either by sulphonylurea and metformin therapy or sulphonylurea therapy alone. There was no significant difference in blood glucose concentration between the two groups although serum insulin concentration was significantly higher in the group treated by sulphonylurea therapy alone. Concentrations of several intermediary metabolites were higher when metformin formed part of the therapy. Thus, mean blood lactate, pyruvate, alanine and total ketone body concentrations and the lactate/pyruvate ratio and 3-hydroxybutyrate/acetoacetate ratio were all significantly elevated during sulphonylurea and metformin therapy. It is concluded that the use of metformin with a sulphonylurea results in widespread abnormalities in blood concentrations of intermediary metabolites.

Adult↗
PubMed1979

Metabolic studies during normoglycaemic clamping of insulin-dependent diabetics using a glucose-controlled insulin infusion system.

Metabolic rhythms have been studied in six insulin-dependent diabetics during subcutaneous insulin therapy, and during control of blood glucose concentration by a glucose-controlled insulin infusion system (GCIIS). In none of the subjects was blood glucose concentration consistently within the normal range during subcutaneous insulin therapy. In contrast, blood glucose concentration was within the normal range after 3.5 h of insulin delivery by the glucose-controlled insulin infusion system and remained in the normal range for the following 8 h through lunch and dinner. Mean blood glucose concentration during this time ranged from 5.31 to 7.90 mM. Following normalisation of blood glucose concentration, blood lactate and pyruvate were similar with both the GCIIS and subcutaneous insulin therapy. Post-prandial lactate peaks were delayed with the GCIIS. Alanine levels were consistently higher during control with the GCIIS compared with subcutaneous therapy, while blood ketone body and plasma NEFA levels were lower, and the premeal peaks in the lipid metabolites were delayed. It is not possible to conclude that attainment of normoglycaemia with the present generation of glucose-controlled insulin infusion systems in insulin-dependent diabetics is accompanied by total normalisation of intermediary metabolism.

Adult↗
PubMed1978

A glucose-controlled insulin infusion system for diabetic women during labour.

A glucose-controlled insulin infusion system was used to control blood glucose concentration during labour or caesarean section in six insulin-dependent diabetics. The mean blood glucose concentration during the four hours of labour immediately before delivery was 4.6-5.2 mmol/1 (82.9-93.7 mg/100 ml). Feedback control of insulin delivery by blood glucose concentration should decrease the risk of postpartum hypoglycaemia in the infant and allow normal obstetric management for the insulin-dependent diabetic in labour.

Adult↗
PubMed1978

Biguanides.

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Biguanides↗
PubMed1978

Comparative effects of two doses of glibenclamide upon metabolic rhythms in maturity-onset diabetics.

Five maturity-onset diabetics have been studied during therapy with glibenclamide 2.5 mg and 5 mg by half-hourly blood sampling for twelve hours. All patients had lower mean blood glucose concentrations during therapy with 5 mg glibenclamide. There was no significant difference between serum insulin concentrations on the two doses, however, serum insulin/blood glucose ratio was higher during the larger dose of glibenclamide. Mean blood lactate, pyruvate and serum triglycerides were significantly lower, and blood glycerol, 3-hydroxybutyrate, and plasma non-esterified fatty acids were increased during therapy with 5 mg. In the individual patient the changes in blood glycerol and plasma non-esterified fatty acids were related to changes in circulating insulin concentration and did not appear to be a true extra-pancreatic effect of glibenclamide. The mechanism of any extra-pancreatic effect remains unclear.

Aged↗
PubMed1978

Hyperlactatemia in diabetics with retinopathy during combined sulphonylurea and phenformin therapy.

Blood lactate concentration has been measured at intervals over a twelve hour period in four maturity-onset diabetics with retinopathy treated by sulphonylurea and phenformin therapy. Despite moderately good control of blood glucose, all four patients had markedly elevated concentrations of blood lactate (12h means of 2.1-2;4 mmol/1) with concentrations greater than 3 mmol/1 at some time during the day. Hepatic function was normal in all patients and in all four patients plasma creatinine was 80-85 mumol/1, (normal range 60-125 mumol/1) so that the usual indications for not using biguanides were absent. It is concluded that diabetics with retinopathy constitute a group of patients with an increased risk of phenformin-associated lactic acidosis, and that plasma creatinine estimation may be unreliable in assessing whether patients are suitable for phenformin therapy.

Aged↗
PubMed1977

Lactic acidosis.

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Acetates↗
PubMed1977

Comparative effects of phenformin, metformin and glibenclamide on metabolic rhythms in maturity-onset diabetics.

Twelve hour metabolic rhythms have been performed on six maturity-onset diabetic subjects during successive periods of therapy with phenformin, metformin, and glibenclamide. Moderate control of blood glucose concentration was achieved with phenformin and metformin, the lowest concentrations being found with glibenclamide. Mean blood lactate concentration was grossly elevated during phenformin therapy, moderately elevated with metformin and normal during glibenclamide treatment. Similar patterns were found for the lactate/pyruvate ratio, alanine, glycerol and ketone bodies. Serum triglyceride concentrations were significantly higher during phenformin treatment than with the other two regimes. Serum insulin concentration was higher on glibenclamide than with either biguanide. Most of these effects of the biguanides could be accounted for by an inhibitory effect on hepatic gluconeogenesis. It is concluded that the use of biguanides as hypoglycaemic agents in diabetes is associated with the production of multiple metabolic abnormalities.

Aged↗