Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hyperglucagonemia that occurs in vivo in animals made diabetic with alloxan or streptozotocin is not suppressed by high glucose but is suppressed by exogenous insulin. These observations together with other studies suggested that insulin-dependent glucose transport and metabolism by the alpha-cells serves as the primary mechanism controlling glucagon secretion. This hypothesis was tested in the present investigation. The possible interactions between glucose, insulin, and a mixture of 20 amino acids at physiological proportions were examined in the isolated-perfusin diabetic rats. Release of insulin and glucagon were used as indicators of theta-cell and alpha-cell function. According to rigid criteria the diabetic animals entering the study were severely diabetic. It was found that in vitro: (a) basal glucagon release (measured in the absence of an alpha-cell stimulus or inhibitor) was extremely low, even lower (i.e. 10%) than the basal rates seen in controls; (b) the alpha-cells of alloxanized- and streptozotocin-treated rats responded with a biphasic glucagon release to stimulation by an amino acid mixture; (c) this alpha-cell response was reduced after both streptozotocin and alloxan; (d) glucose at 5 mM was a potent inhibitor of amino acid-induced glucagon secretion in both types of experimental diabetes; (e) in alloxan diabetes alpha-cell stimulation by amino acids can be curbed by exogenous insulin, whereas glucagon secretion by the perfused pancreas of streptoxotocin diabetic rats appeared to be resistant to insulin action. The data indicate that the modulation of glucagon secretion by glucose in vitro is indipendent of insulin and that other unknown factors extrinsic to the pancreatic islets are responsible for the hyperglucagonemia observed in vivo.
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PMID:Insulin and glucose as modulators of the amino acid-induced glucagon release in the isolated pancreas of alloxan and streptozotocin diabetic rats. 12 28

Near term fetal monkey livers were perfused with a closed recirculating system and a defined perfusion medium. Livers from normal fetal animals were able to release glucose rapidly into the perfusate when they were exposed to glucagon, cyclic AMP, or an aglycemic perfusate, but they did not remove glucose rapidly from the perfusate, synthesize glycogen, or activate liver glycogen synthetase in response to hyperglycemia (Figs. 1,2, and 3; Table 1). Insulin decreased glucose mobilization in response to aglycemia, but did not stimulate glucose uptake during hyperglycemia; insulin activated glycogen synthetase (Table 1; Figs. 1 and 3). Livers from fetuses of streptozotocin-treated mothers and livers from 2-week-old neonates released more glucose into the perfusate in response to aglycemia then did livers from normal fetal monkeys (Fig. 4). These observations support the possibility that neonatal monkey liver is capable of rapidly mobilizing glucose during periods of hypoglycemia but is unable to take up glucose and store glycogen rapidly during periods of hyperglycemia.
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PMID:Glucose regulation by isolated near term fetal monkey liver. 12 68

In carps living since 4 months at 6, 20 or 30 degrees C, epinephrine or glucagon injections produce increase in plasma glucose but affect only slightly liver glycogen: lower is the temperature, slower and longer are the effect. Insulin injection induces more or less delayed hypoglycaemia according to temperature acclimatization; decrease in blood glucose is accompanied by a slight increase of glycogen in all tissues at 6 degrees C and on the contrary by a very strong depletion of this polysaccharide in liver and even heart at 20 and 30 degrees C.
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PMID:[Effect of adrenaline, glucagon and insulin on glucose metabolism in carp: influence of temperature]. 12 34

Adult goats of a white breed were injected i.v. with glucagon in doses of 6.25--25 mug/kg. The blood sugar curve rose relatively slowly after the injection after the injection and the maximum increase, which attained 360--400% of the resting value was usually recorded 20-30 min after glucagon administration. The non-esterified fatty acid (NEFA) level rose immediately after injecting glucose. Within 10 min it returned to the initial value and then fell abruptly. No concentration correlation was found between the glucagon dose and the size of the metabolic response.
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PMID:Effect of glucagon on glucose and fatty acid metabolism in goats. 12 16

Islet isografts were injected into the portal veins of rats made diabetic with streptozotocin. The isografts normalized not only plasma glucose and insulin levels but also the elevated plasma immunoreactive glucagon level. The in vitro basal insulin secretion and prompt sensitivity to glucose were shown directly by perfusing isolated livers containing transplanted islets. In vitro glucagon secretion to an arginine stimulus could not be demonstrated, although it would have been expected demonstrated, although it would have been expected in normal islets. Thus, it appears that insulin derived from transplanted islets is capable of correcting endogenous hyperglucagonemia and of ameliorating the effects of experimental diabetes while transplanted islet glucagon secretion is relatively suppressed.
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PMID:Islet transplantation into rat liver: in vitro secretion of insulin from the isolated perfused liver and in vivo glucagon suppression. 13 Oct 32

One hour following intravenous streptozotocin, rat pancreases were perfused in situ, and , in contrast to saline-injected controls a marked decrease of insulin secretion was observed. In these streptozotocin-treated animals, baseline glucagon secretion was enhanced when the perfusate glucose concentration was either 80 mg./100 ml. or 300 mg./100 ml. In addition there was hypersecretion of glucagon in response to arginine. Exogenous insulin (20,000 muU./ml.) could suppress glucagon secretion when endogenous secretion was plentiful. Baseline and arginine-stimulated glucagon secretion of the streptozotocin treated animals was not suppressed by large amounts of glucose and insulin to the degree seen in control animals. The glucagon rise in response to an abrupt fall of glucose from 80 mg./100 ml. to 25 mg./100 ml. was not significantly higher in the control group than in the streptozotocin group. The results seen with epinephrine were in sharp contrast to those found with arginine. Epinephrine-stimulated glucagon secretion was not enhanced in the streptozotocin group. In addition, epinephrine-induced secretion could be suppressed by exogenous insulin in both the control and streptozotocin groups. The differences may be secondary to differences of endogenous insulin secretion. The present results are compatible with the hypothesis that local insulin secretion can exert a significant suppressive effect upon the alpha cell and that the inhibition of glucagon secretion by glucose is partially mediated by this mechanism. Furthermore, anomalous local insulin secretion may contribute to the abnormal glucagon secretion of diabetes mellitus.
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PMID:Glucagon secretion from the perfused pancreas of streptozotocin-treated rats. 13 25

Glibenclamide stimulates the insulin secretion by the isolated and perfused rat pancreas, but does not inhibit glucagon secretion when the perfusion liquid contains 1.5 g/I glucose. In the absence of glucose in the perfusion medium, glibenclamide stimulates both insulin and glucagon secretions.
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PMID:[Action of glibenclamide on glucagon and insulin secretions studied on isolated and perfused pancreas of the rat]. 13 49

Recovery from diabetes was observed in streptozotocin-treated mice that received subcutaneous, isogeneic transplants of duct-ligated pancreas. Transplants excised from recovered hosts contained both immunoreactive insulin (IRI) and glucagon (IRG), indicating that both A and B cells capable of hormone storage were present. The IRI content in transplants, although only one sixth of that transplanted 6 wk earlier, was still 21/2 times greater than that in the host pancreas and was inversely related to the plasma glucose of the recipient during and after recovery. The IRI content in the transplant added to that in the host pancreas totaled 13% of the IRI found in the normal mouse pancreas, which sufficed for over-all recovery from diabetes but was insufficient to provide normal glucose tolerance and insulin response to a major glucose challenge. The abnormally high content of glucagon noted in the pancreas of hyperglycemic, sham transplanted mice was reduced by one-half in the pancreas of those transplanted mice returning to normal plasma glucose and insulin. Thus, the insulin content of the transplant was important to the recovery of isografted mice, but in addition, and perhaps as a consequence of recovery, there was a slight increase in the insulin storage capacity of the host pancreas and a marked reduction of glucagon compared to the content of these hormones in the pancreas of hyperglycemic, sham transplanted mice.
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PMID:Subcutaneous, isogeneic transplantation of duct-ligated pancreas in streptozotocin diabetic mice: relationships between recovery and hormone contents in transplants or host pancreas. 13 45

Fasting blood glucose (FBG), serum immunoreactive insulin (IRI), plasma immunoreactive glucagon (IRG), body weight, and caloric intake were measured in long-term islet-isografted rats eight to 10 months following intraperitoneal islet transplantation in in age-matched, sham-operated, concurrently followed normal and diabetic controls. Islet recipients had normal body weights, but they were significantly polyphagic, hyperinsulinemic, and hyperglucagonemic when compared with normals. Fasting blood glucose levels were reduced by 10 per cent. Several factors may be related to the occurrence of these abnormalities in long-term islet-isografted rats, including (1) the mass of islets transplanted, (2) the age of donor tissue, (3) the heterotopic location of islet grafts, and (4) the lack of normal innervation of transplanted islet cells.
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PMID:Hyperinsulinemia and hyperglucagonemia following pancreatic islet transplantation in diabetic rats. 13 3

The intraportal injection of 350 to 1,000 isolated islets into streptozotocin-diabetic rats immediately normalized (approximately 24 hours) fasting plasma glucose and insulin levels. Polyuria, polydipsia, and hyperglucagonemia disappeared more gradually over a 2-to-12-week period--the time required for normalization varying with the severity of the diabetes and the number of islets transplanted. In long-term islet-transplanted rats (greater than five months), the hepatic insulin and glucagon reserves averaged 50 per cent and 25 per cent, respectively, of the corresponding normal pancreatic hormone content. Glucagon was increased slightly in the pancreas of streptozotocin-diabetic rats and decreased considerably in transplanted animals. However, total pancreatic glucagon (i.e. pancreatic and hepatic reserves) in transplanted animals was the same as the pancreatic content of normal control rats, indicating the presence of feedback control mechanism(s) in the regulation of pancreatic glucagon reserves. Long-term transplanted islets demonstrated well-granulated A-, B-, and D-cell movement out of the vascular space and the formation of narrow intercellular spaces and junctional complexes with surrounding hepatocytes.
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PMID:Metabolic and morphologic studies in intraportal-islet-transplanted rats. 13 76


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