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

A patient with functioning islet cell carcinoma is described who had amelioration of her hypoglycemia during the development of ectopic ACTH syndrome. Moon facies and hyperkalemic metabolic acidosis were also present in this patient, features uncommonly seen in the actopic ACTH syndrome. At autopsy, she was found to have active tuberculosis. Prophylactic antituberculous therapy should be given to high-risk patients with the ectopic ACTH syndrome. High doses of ACTH may be palliative in refractory hypoglycemic states.
Diabetes 1975 Jun
PMID:Amelioration of hypoglycemia in a patient with malignant insulinoma during the development of the ectopic ACTH syndrome. 23

Exercise, an important component of good diabetic control, is often associated with hypoglycemia in insulin-treated patients. Understanding the mechanism of exercise-induced hypoglycemia and its relationship to the insulin injection site will be helpful in the management of diabetes.
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PMID:Exercise and diabetic control. 24 9

These experiments have been designed to study the influence of alanine infusion of glucose dynamics in the dog and to further elucidate the role of pancreatic hormones in the interaction of alanine with glucose homeostasis. The primed constant infusion of glucose-2-t was used in order to quantitate the rates of glucose production by the liver (Ra) and glucose utilization (Rd). In a first group of experiments, the intravenous infusion of alanine at the rate of 2 mg./kg./min. produced a moderate enhancement of plasma insulin (IRI), while pancreatic glucagon (IRG) increased more consistently. This different pattern of IRI and IRG response caused the insulin/glucagon molar ratio to decline progressibely throughout the experiment. Both rates of glucose turnover increased significantly during alanine infusion. Since Ra rose more rapidly thanRd did initially, hyperglycemia developed. Later, glucose production slowly decreased and, in spite of the sustained hyperglucagonemia, reached levels very close to the baseline in the second part of the experiment. A significant direct correlation between Ra and IRG was found, while the changes in Ra correlated inversely with those in I/G molar ratio. In a second group of experiments, alanine was infused at the same dose together with 0.4 microng./kg./min. of cyclic somatostatin. In the first part of the infusion, IRG fell more than IRI did, so that I/G ratio increased. Later, IRI levels maintained at low values while IRG returned slowly to the baseline and consequently I/G ratio significantly decreased. Glucose production fell rapidly soon after the beginning of the infusion, and therefore hypoglycemia developed. Later, Ra increased progressively to levels above baseline and plasma glucose returned to the preinfusion levels. As in the the first group of experiments, a significant direct correlation between Ra and IRG and an inverse correlation between the changes in Ra and I/G ratio were observed. These experiments demonstrate that alanine infusion produces an acceleration of glucose turnover and that a clear interrelationship between the release of glucose by the liver and the mobilization of pancreatic hormones exists. Finally, the experiments with somatostatin indicate that hyperglucagonemia is one of the mechanisms underlying the stimulatory effect of alanine on glucose production.
Diabetes 1977 Apr
PMID:Studies on the mechanism underlying the influence of alanine infusion on glucose dynamics in the dog. 30 Mar 41

To investigate the development of diabetes mellitus in patients with thalassemia major, plasma glucose and immunoreactive insulin (IRI) levels following oral glucose and intravenous tolbutamide and glucose disappearance rates following intravenous insulin were measured in 10 patients before and during five years on a high transfusion program (HTP). Plasma immunoreactive glucagon (IRG) levels following oral glucose, intravenous insulin, and arginine were measured during the sixth year. Serial percutaneous liver biopsies were performed on seven patients. The oral glucose tolerance tests (OGAT) and mean peak IRI levels were normal in nine of 10 patients before HTP. After HTP was begun a progressive deterioration of OGTT occurred despite normal IRI levels. Following tolbutamide, the mean per cent fall in plasma glucose in the patients before HTP was significantly less than in controls (p less than 0.01) and similar to that of controls during five years of HTP in spite of higher than normal peak IRI levels. Of seven survivors after six years of HTP, three had normal OGTT and four had chemical diabetes; mean peak IRI levels were normal, but fasting IRG levels were significantly higher than in controls (p less than 0.05). In all seven patients, plasma IRG failed to increase following insulin-induced hypoglycemia and was significantly higher than in controls after arginine (p less than 0.01); after oral glucose, plasma IRG fell significantly below that of fasting only in the patients with chemical diabetes (p less than 0.03). Following intravenous insulin, the mean per cent fall in glucose before and during HTP was significantly less than in controls (p less than 0.01). Hemosiderosis and cirrhosis were present in all biopsied patients. Four patients died; two had chemical and two had nonketotic insulin-dependent diabetes. These data suggest that diabetes mellitus occurs frequently in patients with thalassemia on HTP and that insulin resistance and hyperglucagonemia, possibly due to cirrhosis, are important etiologic factors.
Diabetes 1977 Mar
PMID:Carbohydrate metabolism and pancreatic islet-cell function in thalassemia major. 32 76

The authors examined 48 patients with different endocrine pathology (relatives of patients with diabetes mellitus with a normal glucose tolerance test, patients with diabetes mellitus, obesity, thyrotoxicosis, and hypothyroidism) and a group of healthy persons. Blood glucagon concentration was determined radioimmunologically on fasting stomach and against the background of insulin hypoglycemia. A marked reduction of glucagon on fasting stomach was noted in patients with diabetes mellitus, and a reduction of the hormone concentration 30 and 60 min after the insulin injection. In obese patients and relatives of diabetic patients the initial blood glucagon level was not different from that in healthy persons. At the same time there was a significant reduction, and in relatives of diabetes patients also a retardation of glucagon secretion against the background of insulin hypoglycemia. The pattern of glucagon secretion in thyrotoxicosis and hypothyroidism proved to be changed.
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PMID:[Glucagon secretion in several endocrine diseases]. 36 65

Comparisons are made between the incidence, prognosis and treatment of juvenile-onset diabetes and other endocrinopathies in the young. 548 patients with insulin deficient diabetes diagnosed before 20 years of age have been reviewed. Excess mortality, especially at 35--40 years of age was found. Profiles of blood glucose and serum insulin have been studied and compared to those of normal subjects. The variation of insulin absorption and effect of insulin antibodies on the free insulin levels achieved after exogenous insulin injections have been demonstrated. The common occurrence of nocturnal subclinical hypoglycaemia following intermediate or long-acting insulin was often found to be the cause of poor diabetic control. Five out of 33 patients with 'difficult' diabetes had an unexplained resistance to high levels of free-insulin. The value of self-monitoring and HbAl measurements in the improvement of diabetic control and possibly life expectation is reviewed. The incidence of thyroid disease was found to be increased in 1779 insulin deficient diabetics of all ages and persistence of islet-cell antibodies suggests that the diabetes may be due to autoimmunity in some of these patients.
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PMID:Insulin deficient diabetes. Contrasts with other endocrine deficiencies. 36 58

The effects of physical activity on blood glucose homeostasis in diabetes mellitus and the potential benefits of exercise in the treatment of diabetic patients, are reviewed. Mild physical exercise results in a fall of blood glucose levels in controlled diabetic patients; this acute effect of exercise might be used in particular to inhibit the rise of blood glucose seen in insulin-treated diabetics after food intake. In contrast, physical activity will further deteriorate the metabolic situation in decompensated diabetic patients by an increase in blood glucose and a rapid aggravation of ketosis. On the other hand exercise potentiates the blood glucose lowering effect of subcutaneously injected insulin; therefore precautions have to be taken in order to avoid hypoglycemia in insulin-dependent diabetics especially during and after more strenous exercise. In juvenile-type diabetes, physical activity can be used as an efficient therapeutic adjunct only in cooperative, well-instructed patients who are used to check their metabolic situation on a regular basis. Physical training increases the tissues' sensitivity towards (endogenous) insulin. Hence, in addition to the diet, training might represent the most appropriate treatment in maturity onset-type diabetic patients. However, direct evidence for an improvement of glucose tolerance in diabetic patients by physical training is still lacking. In order to formulate detailed, generally applicable recommendations on how to carry out a useful therapeutic program of physical exercise and/or training in diabetic patients, further clinical studies assessing the quantitative effects of physical activity on carbohydrate metabolism are needed.
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PMID:The role of physical exercise and training in the management of diabetes mellitus. 37 13

The present status of knowledge about glucagon pathophysiology in diabetes is reviewed. 1) A-cells behave abnormally in all varieties of diabetes mellitus, spontaneous and experimental, except perhaps in case of pancreatectomized humans. These abnormalities are : hyperreactivity of A-cells to arginine, non suppressibility by glucose, and absence of stimulation following hypoglycemia. 2) These abnormalities appear as secondary in most instances : a) A-cells behave in a normal way in most studies with prediabetics ; b) plasma glucagon concentration is normalized by excellent control of diabetes or following prolonged insulin infusion. High doses of insulin are required most of the times to obtain a normalization of A-cell function : in insulin-dependent diabetics, the physiological portoperipheral insulin gradient no longer exists, and the high doses of insulin which are necessary may be the only mean to reconstitute the high insulin concentrations supposed to be present at the A-cell level. 3) Conflicting results have been collected about the role of this glucagon excess in aggravating the diabetic metabolic syndrome. Evanescent effects follow sustained glucagon infusions: but in diabetics, glucagon bursts rather than permanent hyperglucagonemia are observed and these appear deleterious to glucose tolerance. It seems clear however that insulin deprivation is required for the full expression of the consequences of glucagon excess.
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PMID:Glucagon and diabetes mellitus. 37 65

Control of diabetes from complete normalisation to less adequate degrees of metabolic regulation needs to be assessed with regard to conditions of evaluation and to severity of the disease. Under optimal conditions the therapeutic events should occur with well-timed regularity. Different assessment criteria are appropriate depending on the severity of the deficiency of endogenous insulin. Plasma and urine glucose and ketone body measurements remain the practical standards for assessing diabetic control. Abnormalities of lipid and protein metabolites serve to augment the scope of the assessment. Triglycerides and haemoglobin AIc are also useful indicators of control. In mild (Type II) diabetes it may be possible to achieve normal plasma glucose measurements two hours after meals. Such aims carry a risk of hypoglycaemia in severe (Type I) diabetes. Normoglycaemia and aglycosuria in severe diabetes are feasible only preprandially in most cases. The use of urine glucose tests requires evaluation of blood-to-urine glucose relationships. Practical and convenient methods for identifying patients with high or low "renal thresholds" are described. Investigational methods for characterising diabetic patients assess the variability of glucose and other variables during therapy, as well as the degree to which normal values are attained. Such assessment methods may gain increasing practical importance as therapeutic approaches to diabetic control which are experimental at present come into practice.
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PMID:Methods of assessing diabetic control. 38 Oct 83

In a survey, the pharmacological and clinical documentation of metformin is presented and discussed, and the present state of knowledge relating to metformin-associated lactic acidosis is reviewed. The use of metformin in the treatment of diabetes is based on clinical experience over twenty years. It has been well documented that metformin is effective in maturity-onset diabetes both as monotherapy and in combination with a sulphonylurea. An advantage of metformin treatment is the tendency to weight reduction and the absence of significant hypoglycaemia; blood glucose levels are reduced only to normal. The disadvantages are the gastro-intestinal side effects and the potential risk of vitamin B 12 and folic acid deficiency during long-term use. Metformin-associated lactic acidosis is a very rare complication, which has mainly occured in patients with serious renal insufficiency or other contra-indications to the use of metformin. The association between phenformin and lactic acidosis has led to withdrawal of this biguanide in several countries. Metformin differs from phenformin in certain important respects, and the normal use of metformin does not involve the risk of side effects disproportionate to the intended effect. Further experimental studies are required to substantiate pharmacokinetics and metabolic effects of metformin in man.
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PMID:Metformin: a review of its pharmacological properties and therapeutic use. 38 88


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