Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Somatostatin's release from the isolated rat pancreas was studied using a perfusion technique. Arginine at a concentration of 19 mM produced a biphasic increase in somatostatin release from the perfused rat pancreas. Both first and second phases of somatostatin's increase are significantly higher in the presence of 1 mM theophylline than in the absence of the drug. These results indicate the possible inclusion of the adenylate cyclase--cyclic AMP system in the regulatory mechanism of rat pancreatic somatostatin secretion.
Diabetes 1979 May
PMID:Theophylline: potentiation of arginine-induced somatostatin release from the isolated rat pancreas. 43 74

Glucagon secretion before and during arginine infusions was tested in 11 patients with diabetes associated with haemochromatosis. The results were compared with those obtained in six normal subjects and five patients with haemochromatosis but normal glucose tolerance. The patients with haemochromatosis, regardless of glucose tolerance, exhibited higer level of plasma immunoreactivity for glucagon (antiserum 30-K) suggesting hyperglucagonaemia. However, additional analysis revealed that a considerable amount of this glucagon immunoreactivity was due to cross-reacting material of high molecular weight, the levels of which were significantly higher in patients with idiopathic haemochromatosis. When this was deducted from the total immunoreactivity measured, the resulting values for true glucagon concentrations were similar to those of normal subjects. The data suggest that (1) patients with idiopathic haemochromatosis, whether or not associated with diabetes, exhibit plasma glucagon levels comparable with those of normal subjects; (2) the plasma of the same patients contains significantly more high-molecular-weight substances reacting with glucagon antiserum 30-K than is present in plasma of normal subjects; and (3) 'hyperglucagonaemia' may be erroneously suggested when glucagon is measured with certain antisera reputed to be specific for glucagon.
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PMID:Plasma glucagon in diabetes of haemochromatosis: too low or too high? 43 52

Frequent transfusions improve the general well being in patients with beta-thalassemia major but carry the risk of iron intoxication including the development of diabetes mellitus. Of 22 patients with beta-thalassemia major (age 3-17 years) only 3 had a normal oral glucose tolerance. The remainder had either borderline or moderately pathological glucose curves. The mean glucose concentration was increased, and the mean insulin concentration and insulin/glucose ratio were diminished. In contrast to the oral test, the i.v. glucose tolerance test gave pathological results in only 2 of 16 patients tested. The i.v. glucose test thus may be less selective than the oral test. The mean insulin concentration was lower also after intravenous glucose, but the early insulin peak was preserved. Arginine infusion led to a normal insulin and growth hormone release. This moderate impairment of insulin release found in most of the patients leaves the hope that an efficient chelating therapy scheme might reverse beta-cell dysfunction.
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PMID:Increased risk of diabetes mellitus in beta- thalassemia major due to iron overload. 50 Mar 81

Changes in the serum level of growth hormone have been studied in 28 diabetics (6 exhibiting no diabetic retinopathy (d. r.), 10 displaying a non proliferative d. r., 6 having proliferative d. r., and 6 Brittle-diabetes) together with a control group consisting of 11 subjects (5 being totally healthy, and 6 having acromegaly without d. r.). Blood samples were obtained before and after arginine and glucagon administration and also following controlled exercise on the ergometer with 50% of the actual working capacity during 20 minutes. The presence of d. r. and its stage has been determined by fluorescein angiography. Our results demonstrate that an increased secretion of growth hormone in diabetics actually constitutes a manifestation of metabolic instability. Apparantly no correlation exists between the appearance of d. r. or its stage and the degree of growth hormone release.
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PMID:[Growth hormone and diabetic retinopathy (author's transl)]. 63 68

In the course of familial idiopathic haemochromatosis with diabetes, after stimulation with arginine, the alpha cell responds perfectly to stimulation, in contrast to the case of chronic pancreatic diseases. After an oral glucose load, there is no reduction in plasma glucagon concentrations, and a paradoxal increase is sometimes seen. These results are quite similar to those reported in common diabetes. Secretion of growth hormone after an infusion of arginine and insulin hypoglycaemia seem to be significantly reduced in comparison with normal subjects and those suffering from common diabetes, paired and explored using the same protocol. This may perhaps explain the low degree of severity and slow course of associated vascular disease.
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PMID:[Familial idiopathic haemochromatosis with diabetes. Study of glucagon and growth hormone secretions (author's transl)]. 63 72

In a group of pancreatectomized subjects, immunoreactive glucagon (IRG) concentrations were normal after an overnight fast, increased after oral glucose, were not suppressed by somatostatin (SRIF) or insulin, and in two of four subjects they rose with an arginine infusion. Even though the SRIF infusion failed to lower IRG, there was a fall in plasma glucose concentration in both subjects. In two subjects, endogenous hyperglycemia occurred during insulin withdrawal without a rise in IRG, and, in one subject, mild diabetic ketoacidosis developed with only a minimal rise in IRG. These results support the presence of an extrapancreatic source of IRG in man. Secretion from these extrapancreatic alpha cells appears to be regulated differently than secretion from pancreatic alpha cells.
Diabetes 1978 Oct
PMID:Immunoreactive glucagon responses to oral glucose, insulin infusion and deprivation, and somatostatin in pancreatectomized man. 70 Feb 56

The role of calcium transport into the pancreatic A2-cell in release of glucagon was studied in the perfused in vitro rat pancreas exposed to the organic calcium-antagonist verapamil (10 and 20 microns). As judged by the inhibitory effect of verapamil, a sufficient influx of calcium was required for glucagon release to be stimulated by either arginine (10 mM) or a lowering of the glucose concentration from 16.6 to 3.3 mM. However, such was not the case for glucose to inhibit the release of glucagon or when the A-2-cell was established in a stimulated state during prolonged exposure to a low, 3.3 mM, glucose concentration. These findings suggest that the role of inwardly directed transport of calcium in the secretory process of the A2-cell is of a complex nature, being dependent on the type of stimulus employed (arginine or glucose) and, in the case of glucose, on the static or dynamic state of the cell. The intimate mechanisms by which calcium exerts such complex effects on the secretory process in the A2-cell remain to be elucidated.
Diabetes 1978 Oct
PMID:The role of calcium in glucagon release. Studies with verapamil. 70 Feb 62

Growth hormone injected daily in 6 dogs for 6 days caused a 20-fold elevation in fasting serum immunoreactive insulin (IRI) without appreciable change in serum glucose in 1 day. In the somatotrophic diabetes that occurred after 2 days, the hyperinsulinaemia was maintained and the serum IRI/glucose (I/G) ratio declined from the early high level but remained elevated. During this treatment, in response to glucose infusion, the rise in serum IRI above the initially high fasting level was 16 times the normal. In response to glucagon, the rise in IRI was twice the normal and the rise in glucose was more prolonged, resulting in a decline in the I/G ratio. In response to arginine infusion, the rise in serum IRI was 8 times the normal and the rise in the I/G ratio was twice normal. Following a meal, the rise in serum IRI was 8 times the normal. Thus, with growth hormone treatment the insulin secretory responses to these stimulating factors were magnified over the already elevated fasting level of secretion. The insulin content of the pancreas was reduced to less than 10% of normal by growth hormone treatment for 6 days, due apparently to elevation of the rate of secretion over the rae of formation of insulin.
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PMID:Somatotrophic diabetes: insulin release responses to arginine and glucagon in dogs. 70 Feb 82

The relationship between two metabolites free fatty acids (FFA) and amino acids (AA), and the two main pancreatic hormones, insulin and glucagon, was studied by infusing small amounts of these metabolites into normal and diabetic Peking ducks, i.e. two days after subtotal pancreatectomy. Infusion of oleic acid (0.365 g/kg/30 min as an emulsion in plasma) indicated a suppressive effect of free fatty acids on glucagon secretion, but was without effect on insulin secretion, in normal as well as in diabetic ducks, indicating that insulin might not be directly involved in the FFA-glucagon feedback in the duck. Infusions of arginine for one hour (1 g/kg/h) into normal ducks, hyperglycaemic normal birds (as a result of glucose infusion: 1 g/kg/h) and diabetic ducks, suggested the persistence of amino acid effect on glucagon secretion, and a slight reduction of the effect on insulin secretion in diabetes. This suggests that insulin may not be involved in amino acid-induced glucagon secretion in the duck.
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PMID:Effect of free fatty acids and amino acids on glucagon and insulin secretions in normal and diabetic ducks. 71 Jul 54

In the anaesthetized fasted non-diabetic male intact rat, alrestatin sodium injected as a bolus (0.75 mmol/kg, i.v.) did not affect basal plasma insulin or glucose levels. However, in response to an intravenous glucose tolerance test, plasma insulin levels were significantly increased above the values observed in the animal during a control test. The decreases in plasma glucose levels after alrestatin were significantly greater than in the control study. In rat pancreatic preparations in vitro, alrestatin lowered the basal release of 3H-norepinephrine and also the release obtained with the catecholamine-releasing agent tyramine. A modulation of catecholamine release appears to be of importance in the mode of action of alrestatin with respect to the insulin secretion and plasma glucose levels. It is suggested that alrestatin may play a useful role in the therapy of diabetes mellitus since it can augment insulin secretion when glucose is administered to a fasted animal in which the acute insulin response has been shown to be like that of the human diabetic, and in addition, can lower arginine-stimulated glucagon secretion in the animal, the latter being a model of an action that is observed in the human diabetic. The net effect of these hormonal changes has been predicted previously to be a lowering of the blood glucose levels in the human diabetic patient.
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PMID:Effect of alrestatin sodium on glucose-stimulated insulin secretion in the fasted anaesthetized rat. 74 68


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