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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of chronic tolbutamide treatment were examined in a diabetic animal model in which abnormal myocardial function and composition have previously been demonstrated. Eight diabetic dogs were given tolbutamide 250 mg/day orally and compared with seven untreated diabetics, five healthy dogs receiving tolbutamide, and eight normal controls. After one year, resting hemodynamic studies in the intact anesthetized state showed that treated diabetic dogs had a significantly higher left ventricular end-diastolic pressure of 12.1+/-1.3 mm Hg associated with normal end-diastolic volume, compared to 6.1+/-0.8 mm Hg in untreated diabetics (P less than 0.01) and 6.3+/-0.5 in normals. Stroke work and ejection fraction were similar to normals. Acute volume expansion revealed a larger rise of left ventricular end-diastolic pressure in treated and untreated diabetics than normals, without a significant stroke volume response in treated diabetics. Enhanced stiffness of myocardium appeared to be related to interstitial accumulation of periodic acid-Schiff staining material, further intensified in treated diabetics by triglyceride accumulation observed on electron microscopy and by chemical analysis. Thus treatment of diabetes with tolbutamide, despite improved glucose tolerance, effected further reduction of left ventricular function and altered morphology of myocardium.
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PMID:The effects of tolbutamide on the myocardium in experimental diabetes. 83 Feb 9

A method is described for measurement of chlorpropamide, tolbutamide, and the tolbutamide metabolites hydroxymethyltolbutamide and carbotytolbutamide in blood. It consists of formation of the thermally stable methyl-trifluoroacetyl derivatives of chlorpropamide and tolbutamide, and the methyl-heptafluorobutyryl derivatives of hydroxymethyltolbutamide and carboxytolbutamide, which are then analyzed by electron-capture gas chromatography. Measurements of blood levels of the compounds with this method have been verified by quantitation of the same samples using gas chromatography-mass spectrometry in the mass fragmentography mode. Blood level values and beta-phase half-time disappearance rates of chlorpropamide, tolbutamide, hydroxymethyltolbutamide, and carboxytolbutamide were measured in normal volunteers following an oral dose of chlorpropamide or tolbutamide. Blood levels of the four compounds were also determined in a few diabetics receiving continuous daily treatment.
Diabetes 1977 Jan
PMID:Measurement of antidiabetic sulfonylureas in serum by gas chromatography with electron-capture detection. 83 May 65

Thirty-one patients with subclinical diabetes, who showed diabetic or impaired glucose tolerance after treatment for diabetes, were investigated in order to clarify the abnormalities of insulin response in diabetes mellitus. These patients showed a delayed response of plasma insulin during oral glucose loading. In the tolbutamide-glucose test, in which glucose loading followed the intravenous tolbutamide injection at a 60-min interval, the insulin level at 90 min was significantly lowered in a group of 20 patients with subclinical diabetes. In the tolbutamide-glucagon test, in which 1 mg of glucagon was injected 60 min after tolbutamide injection, the maximal level of plasma insulin was significantly decreased in a group of 10 subclinical diabetes except for one patient. These results indicate that insulinogenesis and/or release of insulin were decreased even in subclinical diabetes, suggesting that such a defect in islet function might be one of the abnormalities in primary diabetes.
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PMID:Insulin response to glucose or glucagon in subclinical diabetes previously injected with tolbutamide. 83 36

The effect of sulindac and tolbutamide on the control of diabetes was studied in 12 tolbutamide-treated maturity-onset diabetics with stable glycemic control. After one week of hospitalization on a metabolic ward for adjustment of diet and activity, the patients were treated with sulindac, 200 mg twice daily for one week. The time-to-peak plasma tolbutamide concentration was 3.1, 3.1, and 3.2 hr, respectively, after tolbutamide alone, after the first dose of sulindac, and after sulindac for a week. The areas under the plasma tolbutamide curve were 23.68, 22.10, and 22.78 for the same periods. The half-life for plasma tolbutamide was 7.46, 7.15, and 7.38 hr, respectively. None of the differences were statistically significant. The mean fasting plasma sugar was lower after the sulindac treatment (from 12.5 to 112.9 mg/100 ml, p less than 0.05), but the postprandial values increased slightly (from 137.7 to 142.6). It was concluded that there was no clinically significant interaction between sulindac and tolbutamide.
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PMID:On the question of an interaction between sulindac and tolbutamide in the control of diabetes. 83 41

A 67-year-old female diabetic is presented who developed a Coombs'-positive hemolytic anemia after a year of treatment with tolbutamide. An IgG antibody was identified in the patient's serum that caused the agglutination of both the patient's red blood cells and tolbutamide-coated erythrocytes in the absence of complement. Such a reaction did not occur with the patient's erythrocytes when not exposed to tolbutamide. Agglutination of the patient's serum also occurred with erythrocytes treated with other sulfonylureas (chlorpropamide, glibenclamide, carbutamide) but not with phenacetin.
Diabetes 1977 Feb
PMID:Tolbutamide-induced hemolytic anemia. 83 66

The effect of ethanol on stimulus-induced insulin secretion was studied, and possible mechanisms were examined in fasting unanesthetized and unrestrained rats with indwelling jugular and aortic catheters. Glucose (150 mg.) or tolbutamide (10 mg.) was given rapidly, i.v., one hour after agavage of ethanol or saline (control). Acutely, ethanol treatment caused marked inhibition of glucose-induced insulin secretion and impaired glucose disappearance rate. Tolbutamide-induced insulin secretion was also significantly inhibited, and decline in glucose was significantly less in ethanol-treated rats. In response to ethanol, serum calcium concentration significantly declined for two hours. In another study, an ethanol metabolite, acetate (0.4 micronmole/min.) or vehicle (control) was infused for 60 minutes prior to 150 mg. glucose pulse. Acetate priming significantly potentiated glucose-induced insulin secretion and also improved glucose tolerance. It is proposed that (1) ethanol in vivo acutely induces hypocalcemia, which inhibits glucose- and tolbutamide-induced insulin secretion--which, in turn, causes glucose intolerance and prevents tolbutamide-induced hypoglycemia. (2)Acetate might be the actual petentiating influence on glucose-induced insulin secretion observed several hours after ethanol treatment.
Diabetes 1977 Apr
PMID:Effect of ethanol on stimulus-induced insulin secretion and glucose tolerance. A study of mechanisms. 84 8

A 21-year-old female patient complaining of frequent hypoglycemic attacks in the presence of a large amount of circulating insulin-binding antibodies without previous known immunization is described. In order to clarify the possible mechanism of the hypoglycemic attacks occurring in this new syndrome, changes in plasma glucose, plasma total and free immunoreactive insulin (IRI), and C peptide immunoreactivity (CPR) levels were investigated in the patient before, during, and after a three-hour glucose infusion. The character of her antibodies were also examined. An abrupt discontinuation of the glucose infusion caused a sharp decline in the plasma glucose level, reaching a nadir of 30 mg./100 nk, at 270 minutes; then she became unconscious. A huge amount of total IRI of 2,834 micron U./ml. was registered at 180 minutes, while the peak value of free IRI of 208 micronU./ml. was observed 45 minutes after the cessation of the glucose infusion. Plasma CPR was increased from high basal level, 19.6 ng./ml., to the maximum level of 29.2 ng./ml. The maximum insulin-binding capacity of IgG in the patient's serum was 6.25 mU./ml. The antibody-combining site was homogeneous, showing one high-affinity site (K: 1.1 X 10(9)M-1). Neither the prolonged fasting nor the administration of tolbutamide induced the hypoglycemic attack in the patient. The hypoglycemia may be explained by an unduly excessive amount of insulin liberated from a large pool of bound insulin irrespective of blood sugar level. The cause of the antibody production is also discussed.
Diabetes 1977 May
PMID:Mechanism of hypoglycemia observed in a patient with insulin autoimmune syndrome. 85 50

A case of hyponatraemic coma occurring in a patient with diabetes mellitus treated with tolbutamide is described. Although chlorpropamide is known to cause water retention in some circumstances, this is a less well recognized complication of tolbutamide therapy.
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PMID:Symptomatic hyponatraemia associated with tolbutamide therapy. 87 Aug 94

This neonate developed marked hyperglycemia four days after birth and required insulin therapy for eight weeks. During the acute phase of the disease, immunoreactive insulin was undetectable in portal venous serum. Neither tolbutamide nor theophylline administration significantly triggered insulin secretion. Somatostatin infusion inhibited growth hormone release but had no effect on plasma glucagon or blood glucose concentrations. At 2 1/2 months, two weeks after insulin withdrawal, the infant was still intolerant to an oral glucose load, insulin response was markedly delayed, and growth hormone secretion was paradoxical. At five months, the insulin, glucagon, and growth hormone responses to glucose and to somatostatin were normalized. Thus, in this patient, insulin secretion was transiently deficient. Peculiarities of glucagon and growth hormone secretion were also present but are more characteristic of this age group than of diabetes. The hyperglycemic state was managed by intraportal infusion of 0.1 to 0.2 IU regular insulin/kg/hour. This mode of insulin administration proved efficient, secure, and easy to manage.
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PMID:Transient diabetes mellitus in a neonate. Evaluation of insulin, glucagon, and growth hormone secretion and management with a continuous low-dose insulin infusion. 89 7

In diabetics with different therapy indications the effect of the treatment on the lipid parameters of blood was examined. We estimated the change of the triglycerides, the cholesterol, the free fatty acids and the glycerol depending on the duration of the therapy. We used a combined stimulation test (combination of 100 g glucose, 1.0 g tolbutamide and 1.0 g glucagon in temporary coupling) as method for characterization of the type of diabetes. At the beginning of the therapy the fat parameters mentioned did not differ in patients with exclusively dietetic treatment and in SuH-patients. After longer duration of the therapy in exclusively dietetically compensated patients the fasting glycerol values decreased, were, however, statistically not significant. There were also no essential changes of the triglycerides, the cholesterol and the values of the free fatty acids in the two forms of treatment. The improvement of the carbohydrate tolerance could not be explained with changes of the insulin secretion. The results plead for the fact that the improvement of the diabetic metabolism develops by an increase of the peripheral insulin effectivity. The behaviour of the lipid parameters is not sufficient for an explanation of the carbohydrate tolerance.
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PMID:[Effect of diabetes therapy on the lipid parameters in blood]. 91 May 22


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