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

Conventional insulins contain impurities which are immunogenic; these include pancreatic polypeptide (PP), glucagon and somatostatin and intermediates of insulin synthesis co-extracted during purification. Monocomponent (MC) insulins are free of these contaminants. In 49 insulin-treated diabetic patients, antibodies were found to insulin (94%), pro-insulin (68%) and PP (68%). Antibodies to glucagon and somatostatin were not detected. There was a significantly lower mean maximum binding and titre of insulin and PP antibodies and total circulating insulin (i.e. antibody bound and free) in patients receiving MC insulin. In patients treated with MC insulins for longer than 2 years there was a significant fall in the mean maximum binding of insulin and total serum insulin, but no consistent change in diabetes control and daily insulin dose. It seems that except in the special instances of fat atrophy, insulin allergy and certain cases of insulin resistance, there is no need to resort to MC insulin.
 ...
PMID:Circulating antibodies in diabetics treated with conventional and purified insulins. 69 12

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

Plasma FFA, glucagon, insulin, glucose, and growth hormone were followed every hour during 24 hours of saline infusion, 24 hours of somatostatin (4mg.) infusion, and three hours without infusion in six nonobese and six obese maturity-onset diabetic men. Somatostatin induced the same changes in the parameters of both groups of diabetic patients: A rise in plasma FFA, which gradually disappeared after some hours of infusion, a suppression of plasma glucagon and insulin, and an augmentation of plasma glucose both postprandially and during the night. Plasma growth hormone was suppressed in the nonobese patients, but somatostatin could not further suppress the low and nonfluctuating plasma growth hormone concentration in the obese maturity-onset diabetics. The results indicate that a preparation with a pattern of hormone suppression like that of somatostatin will not be useful in the control of maturity-onset diabetes, because it suppresses insulin and elevates the blood glucose concentration.
Diabetes 1978 Oct
PMID:Somatostatin in maturity-onset diabetes. 70 Feb 57

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

Toxin from the scorpion Leiurus quinquestriatus was used to release norepinephrine from sympathetic nerve endings in the perfused rat pancrease. Addition of toxin, 10 mug./ml., to perfusate containing 0.3 mg./ml. glucose caused a large increase in release of norepinephrine and glucagon. Glucagon secretion was suppressed by perfusate containing 3.0 mg./ml. glucose but still responded to stimulation with scorpion toxin. Atropine, 10 muM, had no effect on either norepinephrine or glucagon release in response to scorpion toxin. The release of glucagon was blocked by 100 muM propranolol, 10 muM phentolamine, or 30 muM phenoxybenzamine. Somatostatin, 55nM, did not affect the release of norepinephrine by scorpion toxin but totally inhibited the glucagon response. These results suggest that pharmacologic stimulation of the adrenergic nerve endings in the rat pancreas can elicit a rapid release of glucagon. This response can be prevented by appropriate concentrations of either alpha or beta adrenergic blocking agents or somatostatin.
Diabetes 1976 Aug
PMID:Stimulation of glucagon secretion by scorpion toxin in the perfused rat pancreas. 78 80

Glucagon is secreted not only by A2-cells of the pancreatic islets but also by A cells in the gastric fundus and duodenum. Several reports have demonstrated that the glucagon plasma concentration is increased in genetic diabetes as well as in many conditions associated with a decreased glucose tolerance such as hepatic cirrhosis, myocardial infarction, infectious diseases, burns, taumatic shock, glucagonomas, acute pancreatitis, acromegaly, pheochromacytoma and Cushing's syndrome. Hyperglucagonemia is particularly important in diabetic ketoacidosis and in non-ketotic hyperosmolar coma. The mechanisms responsible for the diabetic's hyperglucagonemia remain controversial. According to several authors, the increased glucagon secretion is, for its main part, secondary to a prolonged defect in insulin secretion and thus relatively insensitive to an acute insulin administration. According to others, the A cell abnormality is of primary origin, independant from insulin deficiency and its effects are cumulative with those of the insulin lack. Several reports dealing with induced or spontaneous experimental diabetes are in favor of the first or the second hypothesis. It appears likely that glucagon plays a role in the metabolic derangments of diabetes. Indeed, hepatic glucose production is closely related to the ratio of molar concentrations of insulin and glucagon. Finally, in insulin-dependant diabetics, somatostatin infusion reduces plasma glucagon concentration and blood glucose and prevents the development of ketosis after withdrawal of insulin therapy. These results illustrate the contribution of glucagon in the pathogenesis of hyperglycemia and ketosis. Several arguments have been accumulated in favor of the following concept: diabetes hyperglycemia results both from glucose under-utilization secondary to insulin lack and from hepatic glucose over-production due to glucagon excess. Although controversial, the role of glucagon in ketogenesis appears likely.
 ...
PMID:[The role of glucagon in hyperglycemia. A review (author's transl)]. 79 28

Intensive investigations during the last few years have shown that the regulation of the secretion of pancreatic glucagon is controlled by nerval, humoral and metabolic factors. Of decisive importance is the actually present glucose level which by inhibition modifies the effectiveness of the most different stimulators (intestinal hormones, amino acids). In addition to this the hormones insulin and somatostatin formed by the islets of Langerhans of the pancreas seem to be of importance for the local reactivity of the A-cells of the endocrine pancreas. Disturbances of the glucagon secretion of the pancreas have been found in different diseases connected with hyperglycaemia (especially in diabetes mellitus). The review tried to summarize our present knowledge of the physiology and pathophysiology in this field.
 ...
PMID:[Regulation of pancreatic glucagon secretion]. 79 28

To evaluate the role of glucagon in the pathogenesis of diabetic ketoacidosis in man, we studied the effect of suppression of glucagon secretion by somatostatin on changes in plasma beta-hydroxybutyrate and glucose concentrations (as well as changes in their precursors) after acute withdrawal of insulin from seven patients with juvenile-type diabetes. Suppression of glucagon secretion prevented the development of ketoacidosis for 18 hours after acute insulin withdrawal, whereas in control studies mild ketoacidosis occurred 10 hours after insulin was stopped. Plasma beta-hydroxybutyrate, glucose, free fatty acid, and glycerol levels were all markedly lower during suppression of glucagon secretion (p smaller than 0.001), whereas plasma alanine levels were higher (p smaller than 0.001). These studies indicate that insulin lack per se does not lead to fulminant diabetic ketoacidosis in man and that glucagon, by means of its gluconeogenic, ketogenic, and lipolytic actions, is a prerequisite to the development of this condition.
 ...
PMID:Prevention of human diabetic ketoacidosis by somatostatin. Evidence for an essential role of glucagon. 80 37

The effects of thyrotropin-releasing hormone, luteinizing hormone-releasing hormone, substance P, somatostatin, and a partially purified hypothalamic extract on insulin secretion were tested both in vitro and in vivo. Only somatostatin and the hypothalamic extract affected insulin secretion. In vitro, somatostatin decreased glucose-stimulated insulin secretion by isolated islets and in vivo significantly reduced the rate of insulin output into the portal vein. The hypothalamic extract significantly stimulated insulin secretion in both systems. These effects in vivo were independent of glucose concentration. Islets preincubated for four hours responded better in vitro to the hypothalamic extract stimulation and the somatostatin inhibition.
Diabetes 1976 Feb
PMID:Neuroendocrine control of insulin secretion. 81 25

The endocrine function of the pancreas consists of the promotion of storage of nutritive substances after meals through the liberation of insulin and to guarantee the mobilization of this food energy through the secretion of glucagon during fasting. Increased hormone production may result from tumors of the islet cells (insulin: insulinoma; glucagon: glucagonoma; gastrin: Zollinger-Ellison syndrome). An absolute or relative insulin deficiency is a characteristic of diabetes mellitus, in which a relative hyperglucagonemia is also of possible pathophysiological significance. This increased secretion of glucagon can be suppressed by somatostatin. While the clinical application of somatostatin in diabetes mellitus seems problematic at present, the use of a glucose-controlled system of insulin infusion ("artificial pancreas") makes possible a metabolic state approaching the healthy condition.
 ...
PMID:[The endocrine pancreas. From the isolated islet to the "artificial pancreas" (author's transl)]. 81 14


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>