[The "diabetes" nurse can manage the classification of metabolic control better than the patient].
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Biomedical subjects
Publications and source records attributed to S Carlström.
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The postprandial glucose concentrations after a standardized breakfast of 12 type II diabetics were followed and the effect of supplementation of a fibre-containing bulk-purgative (Lunelax) to the meal was investigated. It was found that addition of Lunelax reduced the mean increment glucose concentration with about 9%. The patients reported that Lunelax was convenient to take.
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In a diabetes detection survey carried out between 1962 and 1965, 2477 (1.1%) of 228,883 subjects had Clinistix-positive glucosuria after a carbohydrate-rich luncheon meal. Of these 2477, 578 displayed impaired tolerance to oral glucose without having manifest diabetes. From this group, 267 men were divided into five groups and subjected to the following treatments and controls: (a) diet regulation and 0.5 g tolbutamide t.i.d. (N = 49), annual oral glucose tolerance test (OGTT); (b) diet regulation and one placebo tablet t.i.d. (N = 48), annual OGTT; (c) diet regulation only (N = 50), annual OGTT; (d) no treatment (N = 61), annual OGTT; and (e) no treatment, OGTT at follow-up (N = 59 at follow-up). In addition, a control group was included comprised of men with normal OGTT (N = 52). At follow-up, 29% of those without diet regulation and medication (group e: N = 59) had developed diabetes. Of those on diet regulation, but without active medication (group b plus group c, N = 98), 13% had diabetes. No individual maintaining tolbutamide and diet regulation (N = 23) had progressed to diabetes. In this group, 80% of those later examined (N = 11) had serum tolbutamide concentrations in the therapeutic range. No individual with initially normal OGTT developed diabetes or impaired OGTT. The findings suggest that normal oral glucose tolerance signifies little risk of progress to impaired glucose tolerance and manifest diabetes, whereas impaired glucose tolerance is associated with a high risk of progression to diabetes. In addition, it seems possible that treatment with diet regulation, in combination with tolbutamide, may prevent or postpone progression from impaired glucose tolerance to manifest diabetes.
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The effect of long-term treatment with phenformin and metformin respectively on blood lactate concentrations in relation to submaximal muscular exercise has been examined in 21 maturity-onset diabetics, using a cross-over method. At similar degrees of diabetic control the mean blood lactate concentration during exercise and shortly thereafter was significantly higher when the patients had received phenformin. The mean fasting lactate concentration was 1.07 mmol/l with phenformin and 1.03 mmol/l with metformin and the peak concentration was 2.56 mmol/l and 2.19 mmol/l respectively. The mean fasting blood glucose concentration before the exercise was 11.2 mmol/l with phenformin and 11.3 mmol/l with metformin; the glucose output in the urine during the preceding 24 hours was 93 mmol and 105 mmol respectively. The mean work load during exercise was 60 watts.
The plasma concentrations of free fatty acids (FFA), glycerol and insulin as well as the blood glucose concentration have been followed in two groups of subjects after infusions of theophyllamine. Each individual was examined twice. The 5 subjects in group 2 were given an infusion of norepinephrine before the theophyllamine at one of the examinations and saline at the other. The 6 subjects in group II were given an infusion of norephinephrine at both examinations, followed by theophyllamine on one occasion and by saline on the other. Thus, the subjects in both groups served as their own controls. It was found that theophyllamine caused lipid mobilization, as measured by the plasma FFA and plasma glycerol concentrations, both when given as the only active drug and when given after norepinephrine. The blood glucose concentration rose slightly after norepinephrine and the plasma insulin level increased concomittantly. When theophylline was given as the only active drug, there was no increase in the blood glucose but the plasma insulin concentration rose slightly.
Glucose or corn oil was given perorally to fasting, young healthy volunteers, and the time course of acute effects on lipoprotein lipase activity (LLA) in adipose tissue, plasma glycerol, triglyceride, insulin, and blood glucose levels was followed. After glucose intake, adipose tissue LLA increased rapidly, reaching a maximum of 80 per cent above initial level after 2 h. Plasma glycerol, reflecting the rate of lipolysis of depot lipids, decreased rapidly, temporally well correlated to the LLA changes. After corn oil intake no significant effect on any of the parameters studied was observed except for an increase in the plasma triglyceride level caused by the influx of dietary lipid.
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