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

The isolated perfused canine pancreas with duodenal exclusion was used to examine islet hormone output in response to arginine and exogenous glucagon and insulin. Exogenous glucagon (100 ng/ml) stimulated insulin and somatostatin secretion, which occurred in a biphasic pattern. The insulin response to glucagon was markedly enhanced by increased perfusate glucose, unlike the somatostatin response, which was little affected. The insulin and somatostatin responses were seen between 15 and 45 s after the glucagon stimulus. Pancreatic polypeptide secretion was uninfluenced by exogenous glucagon. Biphasic release of glucagon, somatostatin, and pancreatic polypeptide was evoked by 10 mM arginine, the responses first being apparent within less than 30 s. Exogenous insulin (50 mU/ml) infused for 10 min had no statistically significant effect on glucagon, somatostatin, or pancreatic polypeptide secretion. This study suggests that these four islet hormones may all be involved in the dynamic mechanisms of nutrient metabolism. In addition, potential intra-islet paracrine effects are identified.
Diabetes 1979 Jan
PMID:Somatostatin and pancreatic polypeptide secretion: effects of glucagon, insulin, and arginine. 75 49

To determine if both phases of glucagon secretion are excessive in diabetes, arginine was admimistered intravenously as pulses and as infusions to normal subjects, insulin-dependent diabetics, and noninsulin-requiring diabetics. The acute phase of glucagon secretion, in response to arginine pulses at four different doses (submaximal to maximal alpha-cell stimulating), was indistinguishable in terms of timing, peak levels attained, and total increments comparing controls and diabetics. During the first half of the arginine infusion (500 mg/kg over 30 min) the glucagon rise in controls and diabetics was similar (P greater than 0.1), whereas during the last half of the infusion excessive glucagon levels were seen in the diabetics. No difference in the glucagon responses to arginine administered as either a pulse or an infusion was observed between the two types of diabetics. The acute phase responses of insulin to intravenous, maximal stimulating doses of glucose (20 g) and arginine (2.5 g) were measured in five insulin-independent diabetics. Although the acute insulin response to arginine was normal, there was marked attentuation of the early beta-cell response upon stimulation by glucose. From these results we conclude that although in diabetes excessive glucagon levels are observed with chronic arginine stimulation, the acute phase of glucagon secretion in response to arginine is normal. In addition, the beta-cell in noninsulin-requiring diabetics, although acutely hyporesponsive to glucose, remains normally responsive to another stimulus, arginine.
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PMID:Arginine-stimulated acute phase of insulin and glucagon secretion in diabetic subjects. 78 1

Highly inbred male rats were made diabetic by subtotal pancreatectomy. After diabetes developed, the animals were transplanted with an average of 500 isolated islets, obtained from donors of the same sex and strain, into the portal vein. Groups of islet-transplanted diabetic rats were followed for periods of 3, 6, and 14 months, during which time the performance of the transplanted islets was investigated. Control animals were followed for similar period of time. The findings obtained from each experimental group were integrated so as to provide a continuous picture of the transplanted islet's behaviour from 2 weeks to 14 months post transplantation. To assess islet performance, normal, untreated diabetic, and transplanted animals were subjected to three stimulatory tests of insulin secretion: (1) oral glucose tolerance, (2) intravenous sulfonylurea, and (3) intraperitoneal L-arginine. Normal and transplanted rats were additionally subjected to one inhibitory test of insulin secretion, diazoxide (given orally). At the end of the study, control and experimental animals were killed, and morphological investigations were performed on liver and pancreas. Isotransplantation of islets in partially depancreatized diabetic rats resulted in the reversal of the condition. The transplanted islets were found to respond to physiologic and pharmacologic controls, although the characteristics of the responses were not identical with that of the normal intact islet. The results of this study have suggested that a functional development of the transplanted islets occurs.
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PMID:Long-term function of isotransplanted islets of Langerhans in the diabetic rat. 82 16

The responses of glucagon, growth hormone, and insulin secretion to the oral administration of glucose and to the intravenous infusion of saline, arginine, and insulin were measured in seven patients who had stable diabetes, eight who had unstable diabetes, and seven healthy volunteers. Hyperglycemia suppressed secretion of glucagon in normal subjects but not in diabetics. The oral glucose and arginine infusion tests demonstrated partial preservation of insulin-secretory ability in stable diabetics and its virxual absence in unstable diabetics. Glucagon responses to arginine infusion were similar in all three groups. In response to hypoglycemia induced by insulin infusion, the concentrations of plasma glucagon increased in normal subjects and, to a lesser extent, in stable diabetics but increased in only two of the unstable diabetics. The impairment in glucagon response during hypoglycemia in diabetics correlated positively with the degree of diabetic instability and insulin deficiency during glucose and arginine testing. The severity of the insulin deficiency also correlated with the degree of diabetic instability. These findings support the hypothesis that inherent abnormalities of insulin and glucagon secretion may account for many of the clinical characteristics of unstable and stable diabetic patients.
Diabetes 1977 Jan
PMID:Abnormalities of endogenous glucagon and insulin in unstable diabetes. 83 May 63

Glucagon response to insulin hypoglycemia was tested in diabetics with autonomic neuropathy (N=9), diabetics without neuropathy (N=8), and normals (N=9). With similar levels of hypoglycemia, growth hormone and plasma cortisol increased in all groups. The glucagon response in normals (121+/-19 vs. 308+/-30 pg./ml., mean+/-S.E.M. of baseline vs. hypoglycemia peak) was significantly less in nonneuropathic diabetics than in normals (128+/-13 vs. 209+/-30) and absent in neuropathic diabetes (128+/-23 vs. 115+/-20). Arginine stimulation produced a glucagon response in the neuropathic diabetics (106+/-16 vs. 523+/-103). The data indicate that the capacity to release glucagon during hypoglycemia is lost in diabetic neuropathy while glucagon responsiveness to arginine is retained. Neuropathy in diabetes may contribute to metabolic instability.
Diabetes 1977 Mar
PMID:Lack of glucagon response to hypoglycemia in diabetic autonomic neuropathy. 83 71

In order to investigate the contribution of glucagon to the abnormalities of carbohydrate and lipid metabolism in diabetes, hormones and metabolites were measured in response to IV arginine in 5 juvenile onset (control) diabetics and 5 totally pancreatectomised subjects. In the basal state, both control diabetics and pancreatectomised patients showed abnormally elevated levels of plasma glucose, blood 3-hydroxybutyrate, glycerol and plasma free fatty acids (NEFA), although no glucagon was detectable in the plasma of the pancreatectomised subjects. Blood concentrations of the gluconeogenic precursors alanine and glycerol were higher pancreatectomised patients than in the diabetics. Following infusion of arginine, the rise in glucagon observed in the diabetics was accompanied by a significant increase in plasma glucose and a fall in blood lactate when compared to the pancreatectomised subjects. In spite of the rise in glucagon in the control diabetics, no sigficant change was found in the concentrations of ketone bodies, glycerol or NEFA. Thus glucagon does not seem to have a primary role in producing the metabolic abnormalities of diabetes.
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PMID:Persistent metabolic abnormalities in diabetes in the absence of glucagon. 83 5

Effect of successful treatment on plasma glucagon response to arginine was studied in patients with diabetes mellitus, Cushing's syndrome and hypothyroidism. Exaggerated response of plasma glucagon to arginine infusion in diabetic subjects was normalized in those successfully treated with sulfonylureas and significantly improved in those treated with insulin. Patients with Cushing's syndrome and hypothyroidism also exhibited excessive responsiveness of plasma glucagon, which were completely normalized following treatment. The results suggest that the metabolic derangement is a main etiologic factor in inducing hyperresponsiveness of plasma glucagon to arginine in these disorders.
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PMID:Alteration of plasma glucagon response to arginine after treatment in patients with diabetes mellitus, cushing's syndrome and hypothyroidism. 84 89

The glucagon-secreting potency of 22 amino acids was investigated in the rat isolated perfused pancreas. Arginine and the structurally related amino acids were the most potent A2-cell stimulators that induced a biphasic and sustained glucagon release. Dose-response curver were different for L(+) and D(+)arginine, and the suppressor effect of glucose on the response to L(+) arginine was not detected in the presence of D(+) arginine or homoarginine. Citrulline was the only exception among the arginine-related amino acids; it displayed neither stimulatory nor inhibitory potency on glucagon release. The A2-cell response to D(+) amino acids and artificial analogues of arginine is a strong case for the theory of amino acid receptors' triggering the release of the hormone before (or in the absence of) further metabolism. The prominent rank of arginine and ornithine amont stimulatory amino acids and some other physiologic evidence suggest that A2-cell may play a regulatory role in the metabolsm of ammonia by the liver.
Diabetes 1977 Apr
PMID:Glucagon secretion induced by natural and artificial amino acids in the perfused rat pancreas. 84 11

The effect of arginine infusion on blood sugar and plasma levels of growth hormone and glucagon has been studied in children with clinical diabetes mellitus and in obese children with normal carbohydrate tolerance. Basal levels of plasma GH are significantly lower in obese children than in diabetics and controls; in obese subjects the increment of GH is significantly lower than in diabetics and controls. Basal plasma glucagon levels are comparable in all three groups despite the high sugar levels in diabetic patients. After arginine infusion there is a significant rise in glucagon levels without significant differences between the three groups.
Diabetes 1977 Jun
PMID:Glucagon response to arginine stimulation in obese and diabetic children. 86 26

The contribution of the gastric fundus to the hyperglucagonemia of poorly controlled diabetes was studied in insulin-deprived alloxan-diabetic dogs by simultaneously measuring plasma glucagon in the venous effluents of the fundus and the pancreas, and the inferior vena cavae plasma. In the basal state, mean glucagon averaged 411 +/- 45 pg./ml. in the gastric vein and 941 +/-161 in the pancreaticoduodenal vein; both values were significantly above the vana caval level of 281 +/-35 (p less than 0.01). Intravenous arginine infusion to 1,180 +/- 432 after 1.5 minutes; this was significantly above the mean vena caval glucagon concentration which reached a peak of only 352 +/- 74 (p less than 0.01 to 0.05). Intragastric instillation of arginine was followed by a doubling of gastric vein glucagon within 10 minutes, and the increases in the gastric vein were significantly greater than in the peripheral plasms at several points. The infusion of insulin at a rate of 0.0015 u./kg./min. rapidly lowered glucagon in the gastric and pancreaticoduodenal veins, abolishing the gradient across the stomach and reducing the transpancreatic gradient. The studies raise the possibility that extrapancreatic glucagon may contribute to the hyperglucagonemia of insulin deficiency.
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PMID:Demonstration of gastric glucagon hypersecretion in insulin-deprived alloxan-diabetic dogs. 87 May 72


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