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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight 18-days-postcoitum fetal pancreases were transplanted to isogenic alloxan-diabetic male rats. Some recipients were treated with insulin for seven days immediately after transplantation. Eight animals in both the insulin-treated group and control group were killed 15days after transplantation for morphologic and hormonal studies of the transplanted tissue. Using the morphometric technique of linear scanning, the insulin, glucagon, and somatostatin immunocytochemically positive, cell masses of the fetal pancreatic implants were quantitated. The beta cell mass of the implants from the control animals increased roughly eightfold from the time of transplant; insulin treatment resulted in a further two- to threefold increase. The insulin content of the implants increased more than did the beta cell mass, resulting in the fivefold increase in insulin per beta cell. The alpha cell and delta cell masses did not change during the transplant site, the mass of functional beta cells, and the cell-to-cell content of the implanted tissue. These results are discussed in relation to previous quantitative studies of pancreatic islet cell growth. The relationships of the transplant site, the mass of functional beta cell, and the cell-to-cell interaction within the islet to the maintenance of glucose homeostasis are also discussed.
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PMID:Syngeneic transplantation of fetal rat pancreas. II. Effect of insulin treatment on the growth and differentiation of pancreatic implants fifteen days after transplantation. 35 89

The acute in vitro effect of alloxan on glucagon and insulin secretion from the isolated perfused rat pancreas was examined. Alloxan alone produced transient insulin secretion. Pretreatment with alloxan attenuated both the stimulatory effect of glucose on insulin secretion and the inhibitory effect of glucose on glucagon secretion. Exposure to alloxan in varying doses either partially or completely inhibited insulin secretion induced by arginine in the presence or absence of glucose. On the contrary, pretreatment with alloxan produced complex effects on arginine-induced glucagon secretion. In the absence of glucose, the response of glucagon to arginine infusion was lower in the pancreas exposed to alloxan than in the control experiment. In the presence of glucose, however, an apparently augmented response of glucagon to arginine was observed after exposure to higher doses of alloxan, suggesting an impaired inhibitory effect of glucose on arginine-induced glucagon secretion. These effects of pretreatment with alloxan on glucagon secretion can not be explained by earlier or simultaneous insulin secretion. Therefore, we conclude that alloxan acts not only on beta-cells, but also directly on alpha-cells, although the latter are less sensitive to this agent.
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PMID:Modulation by alloxan of glucagon and insulin secretion in the isolated perfused rat pancreas. 36 31

Eight 18-316 fetal pancreases were transplanted to syngeneic alloxan diabetic male rats. Some of the recipients were treated with insulin for a 7-day period immediately after transplant. By previously published clinical criteria, three groups of recipients could be identified after reversal of diabetes by the transplanted tissue: insulin-treated rapid reversal; insulin-treated slow reversal; and control (not treated with insulin). Five animals in each group were sacrificed after glucose tolerance testing for morphologic and hormonal analysis of the transplanted tissue. The insulin-,glucagon-, and somatostatin-positive islet cell masses of the fetal pancreatic implants were quantitated. There was a correlation between the beta cell mass of the implants and the glucose tolerance exhibited by the host animals. The rapid response insulin-treated recipients had significantly greater implant beta cell mass and insulin content compared with the other groups. There was no difference in implant alpha cell mass among the groups, but the insulin-treated implants had a significantly greater glucagon content. The delta cell mass of insulin-treated rapid response was less than that of the other two groups. The results are discussed in relation to previously reported morphometric analysis 15 days after transplantation. The relationships of transplanted beta cell mass, beta cell differentiation, transplant site, and cell-to-cell interactions within the transplanted islet to the control of glucose homeostasis are also discussed.
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PMID:Syngeneic transplantation of fetal rat pancreas. III. Effect of insulin treatment on the growth and differentiation of the pancreatic implants after reversal of diabetes. 36 28

The aim was to clarify whether or not sudden spike concentrations of plasma growth hormone (GH) can affect the endocrine pancreas in vivo. The peaking of GH was reproduced by an injection (10 mg/kg iv) of bovine GH to anesthetized normal, pancreatectomized, and alloxan-diabetic dogs. In portal but not in peripheral blood, immunoreactive plasma glucagon (IRG), glucagon-like activity (GLI), and immunoreactive insulin (IRI), were significantly elevated within 10 min in normal and alloxan-diabetic dogs. In pancreatectomized dogs, GH did not affect either IRG or GLI. When a physiological dose of GH (6 microgram/kg) calculated to produce ambient peak plasma concentrations of 40 ng/ml was given to four conscious, normal dogs with indwelling portal catheters, a rise of IRG from 108 +/- 19 to 170 +/- 17 pg/ml and of IRI from 20 +/- 12 to 67 +/- 19 muU/ml (mean +/- SE) occurred within 2 min. GLI was not affected. Thus a sudden rise in GH concentration can stimulate the release of a) GLI in the presence but not in the absence of the pancreas, and b) pancreatic IRG and IRI but not extrapancreatic IRG.
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PMID:Effect of growth hormone on acute glucagon and insulin release. 38 Mar 63

The present study provides evidence that changes in glucagon secretion are influential in determining the hyperglycemic activity of catecholamines in normal and diabetic rats. In normal fed rats, epinephrine (EPI) stimulated large increments in glucagon release and inhibited insulin secretion. In contrast, the modest hyperglycemic activity of isoproterenol (ISO) in normal fed rats correlated with its weak glucagon-releasing activity and its strong insulin-releasing activity. In alloxan-diabetic rats, the augmented hyperglycemic response to ISO was accompanied by larger increments in plasma glucagon levels than the catecholamine produced in normal fed rats. When glucagon release was inhibited by a concurrent infusion of somatostatin, the hyperglycemic responses of normal fed rats to EPI were reduced by approximately 67%. ISO-induced hyperglycemia in alloxan-diabetic rats was even more sensitive to inhibition by somatostatin since this response was reduced by approximately 90% when glucagon release was inhibited by somatostatin. These findings indicate that more than half of the hyperglycemic response to EPI in normal fed rats and nearly all of the hyperglycemia produced by ISO in diabetic rats result from increased glucagon release. Moreover, the impotence of ISO as a hyperglycemic agent in normal fed rats is probably due to insulin release which tends to suppress glucagon release.
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PMID:The influence of endogenous glucagon release on hyperglycemic responses to catecholamines in normal fed and diabetic rats. 48 Jan 94

Passaging of the mammary aplastic carcinoma several times in diabetic CBA mice induced an extrapancreatic secretion of glucagon. Consequently, the concentration of immunoreactive glucagon was higher in plasma and the tumor tissue extract. After the injection of alloxan, attempts to reduce the level of this hormone in the diabetic mice were unsuccessful. The tumor cells could have been responsible for the secretion of glucagon.
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PMID:Induction of glucagon synthesis in diabetic CBA mice bearing mammary aplastic carcinomas. 48 Mar 74

In order to investigate secretion of extrapancreatic glucagon in dogs, plasma glucagon and total immunoreactive glucagon (IRG) in response to arginine were determined with antisera specific and non-specific for pancreatic glucagon, respectively. Only a tiny rise of plasma glucagon was observed in the portal vein following arginine infusion performed immediately after total pancreatectomy in a group of 5 normal dogs. In contrast, total IRG in the portal vein increased significantly after arginine infusion even after pancreatectomy. In alloxan diabetic dogs, arginine infusion after total pancreatectomy caused a rise in plasma glucagon in the portal vein, although not significantly. The response of total IRG to arginine in the portal vein was exaggerated in alloxan diabetic dogs. In a group of one-week post-pancreatectomized animals, plasma glucagon and total IRG increased significantly in response to arginine infusion. Furthermore, in these dogs, response of plasma glucagon and plasma total IRG to arginine infusion was abolished after gastrectomy. From the present results it is concluded that secretion of extrapancreatic glucagon increased in response to arginine infusion in the diabetic state, both alloxan diabetic dogs and one-week post-pancreatectomized dogs. In addition, a rise in extrapancreatic glucagon following arginine infusion in the chronically pancreatectomized dogs almost certainly derived from the stomach, as the rise was abolished by gastrectomy.
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PMID:Response of extrapancreatic glucagon to arginine in dogs. 49 57

The present study was designed to examine the effects of intravenously injected alloxan (75 mg/kg) upon plasma somatostatin-like immunoreactivity (SLI), glucagon (IRG), insulin (IRI) and glucose levels in 6 dogs. Within 2 hours of the injection of alloxan, SLI and IRI levels decreased significantly below their respective baselines, while IRG and plasma glucose concentrations increased. At 8 hours SLI levels had increased significantly by 55 pg/ml, together with a rise in IRI and a decrease in IRG and glucose concentrations. After 24 hours, marked hyperglycemia and hyperglucagonemia had developed whereas SLI levels were not different from preinjection values.
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PMID:Response of plasma somatostatin-like immunoreactivity to the administration of alloxan in dogs. 49 95

A decreased plasma glucagon response to insulin-induced hypoglycaemia was found in the normoglucagonaemic alloxan diabetic rat. 0.021-0.240 ng/ml was accepted as the range of normoglucagonaemia. The reduction of the glucagon response was not due to destruction of the alpha 2-cells by alloxan, since a normal response to arginine could be demonstrated. The decreased glucagon response to hypoglycaemia in the insulin deficient normoglucagonaemic alloxan diabetic rat suggests that this alpha 2-cell dysfunction may be caused by insulin lack.
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PMID:Plasma glucagon responses to insulin-induced hypoglycaemia and arginine in normal and alloxan diabetic rats. 52 63

Adenylosuccinase activity of rat liver is depressed by prolonged starvation, cortisol administration, high protein diets, and alloxan diabetes. The loss of activity is not due to the accumulation of a dissociable inhibitor or loss of a cofactor. Starvation produces no loss in activity for 1 day; thereafter the activities of the liver and spleen enzyme decay with a half-life of about 0.9 day. Starvation produces no change in the activity of the kidney, brain, and skeletal muscle enzyme. Refeeding restores the activity of the liver enzyme to the fed level, with only a slight overshoot. The recovery of adenylosuccinase activity is equally rapid after refeeding a balanced diet, or corn oil, or glucose, and is not inhibited by injection of glucagon, in contrast to malic enzyme activity. Recovery is inhibited by cycloheximide, indicating the involvement of protein synthesis. Althouth adenylosuccinase is depressed in liver of starving rat it is elevated in liver of starving chicken. Starvation depresses malic enzyme activity and elevates alanine aminotransferase activity in both species. When rats are starved, the rate of de novo synthesis of adenine mononucleotide decreases in spleen and liver but not in kidney, suggesting a regulatory role for adenylosuccinase in purine biosynthesis. The low activity of adenylosuccinase in liver of severely starved rats is inconsistent with the proposal (Moss, K. M., and McGivan, J.D. (1975) Biochem. J. 150, 275-283) that the purine nucleotide cycle plays a major role in ammonia production for urea synthesis, at least under these conditions.
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PMID:Effect of diet on adenylosuccinase activity in various organs of rat and chicken. 69 Jan 30


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