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 transplantable islet-cell tumor of the golden hamster has already been shown to produce hypoglycemia and hyperinsulinemia in the receptor animal. The present study demonstrates that the plasma pancreatic glucagon concentrations are significantly increased in the tumor-bearing animals but that this hyperglucagonemia is not abolished by administration of glucose or of diazoxide. It is also unresponsive to arginine administrations. In these animals, increased peripheral glucagon plasma concentrations are observed along with a reduced porto-aortic glucagon gradient. Moreover, plasma glucagon in the vena cava is usually higher than that in the aorta and a significant quantity of glucagon is found in the tumor. We conclude that glucagon release from the tumor is in fact responsible for the observed hyperglucagonemia.
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PMID:Glucagon secretion by the transplantable islet-cell tumor of the Syrian hamster. 17 26

The serum levels of total immunoreactive insulin (IRI) and proinsulin-like component (PLC) in the fasting state and following the administration of insulin secretagogues in 5 patients with organic hyperinsulinism and age and sex matched normal subjects are reported. Diagnosis of organic hyperinsulinism could be established in all instances on the basis of the inappropriately high total serum IRI levels for the corresponding blood glucose values; such an abnormal relationship was not seen in normal subjects, and was further enhanced by insulin secretagogues. Unrestrained insulin secretion in organic hyperinsulinism was enhanced following the administration of glucose, tolbutamide, glucagon or amino acids; the last 2 stimuli are known to be ineffective in causing insulin secretion in the presence of hypoglycemia in normal subjects. Four patints had insulinomas and one probably had islet cell hyperplasia or abnormal function of islet cells. Chromatography of serum IRI to quantitate PLC is a useful adjunct to the diagnosis of organic hyperinsulinism as in the fasting state the proportion of PLC is always elevated, above the normal range of 5-22%. Following the administration of insulin secretagogues there was pronounced increase in total serum IRI in organic hyperinsulinism but the proportion of PLC generally decreased, suggesting thereby that mojor increase in IRI was due to release of stored granular IRI which is known to have a low proportion of PLC.
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PMID:Serum and pancreatic immunoreactive insulin (IRI) and proinsulin-like component (PLC), serum IRI and PLC response to different stimuli in normal subjects and organic hyperinsulinism. 18 32

Two sibs who sustained severe hypoglycaemia in the neonatal period are reported. In spite of treatment with frequent feeds intravenous glucose, glucagon, hydrocortisone, and diazoxide, hypoglycaemia persisted, and both infants eventually required subtotal pancreatectomy. Tests for leucine toleranct were normal though the second case showed some protein sensitivity. Histological and immunohistochemical studies indicated nesidioblastosis in both specimens of pancreata. The children are presently performing at mildly retarded levels, and required diazoxide and anticonvulsant medication for some time postoperatively. Because both sexes are represetned, an autosomal recessive inheritance pattern is suggested. The theory of a gut hormone stimulating insulin production is briefly discussed.
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PMID:Idiopathic hypoglycaemia in sibs with morphological evidence of nesidioblastosis of the pancreas. 18 9

Glucagon secretion and its control have been studied in perifused isolated islets of Langerhans of the rat. It was shown that a low concentration of glucose per se does not cause increased glucagon secretion, but that at low glucose concentrations the amino acid arginine stimulates a biphasic secretory response. Such amino acid stimulated glucagon secretion can be suppressed by increasing the glucose content of the perifused media from 1.67 to 5.5 or 16.7 mM; insulin secretion is also then increased. Since high concentrations of added porcine insulin (10 mU/ml) did not affect amino acid stimulated glucagon secretion at low glucose concentration, it was concluded that high concentrations of glucose and not insulin secreted in response to that glucose are probably responsible for suppression of glucagon secretion. At low concentrations of glucose, epinephrine (2.5 X 10(-7) M) also stimulated glucagon secretion. It is concluded that isolated rat islets of Langerhans can be used for the study of glucagon secretion in vitro, and that substances appearing in the blood in vivo at low glucose concentrations are probably responsible for increased glucagon secretion under conditions associated with hypoglycemia.
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PMID:Studies on glucagon secretion using isolated islets of Langerhans of the rat. 18 96

Neonatal hypoglycemia is of frequent occurrence in fasted newborn babies or animals but the origin of this hypoglycemia is not fully understood. Studies performed in newborn rats have shown that liver glycogenolysis and gluconeogenesis occur immediately after birth and that the increase in the activities of key regulatory enzymes (phosphorylase, glycogen synthetase and phosphoenolpyruvate carboxykinase) results probably from the rise of plasma glucagon and the fall of plasma insulin induced by the "stress" of birth. When the liver glycogen stores have been exhausted, i.e. between 6 and 16 hours after birth, a profound hypoglycemia develops in fasting newborn rats. The inability of hepatic gluconeogenesis to produce sufficient glucose to meet the energy requirement of the newborn tissues results from a lack of fat-derived (free fatty acids and ketone bodies) and gluconeogenic (lactate, amino acids) substrates. The stage of appearance and the mechanisms regulating gluconeogenesis in other species including human are discussed.
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PMID:[Energy metabolism in the perinatal period (author's transl)]. 18 42

Effects of endotoxin on carbohydrate metabolism were studied in A/HeJ (endotoxin-sensitive) and C3H/HeJ (endotoxin-resistant) inbred mice. A/HeJ mice developed hypoglycemia within two hours after endotoxin injection, yet liver glycogen content did not differ from controls. Similarly treated C3H/HeJ mice did not develop significant hypoglycemia. Administration of glucagon to endotoxin-treated A/HeJ mice failed to elevate their blood glucose concentrations, while endotoxin-treated mice of the same strain did respond to dibutyryl cyclic AMP with a significant elevation of blood glucose. C3H/HeJ mice on the other hand responded to glucagon and dibutyryl cyclic AMP with elevated blood glucose. Endotoxin-treated C3H/HeJ but not A/HeJ mice were able to carry out gluconeogenesis induced by prednisolone, while both inbred strains showed active glycogenesis after administration of an exogenous glucose load. Administration of glucagon resulted in diminished liver glycogen concentrations in A/HeJ endotoxin-treated mice suggesting no impairment of glycogenolysis. The inability of endotoxin-treated A/HeJ mice to respond to glucagon could be due to impairment of gluconeogenesis. Although endotoxin interfered with the capacity of both inbred strains to respond to glucagon administration with elevation of liver cyclic AMP, the effect was significantly more severe in A/HeJ mice. The susceptibility of A/HeJ mice to the lethal effect of endotoxin may be related to the apparent sensitivity of carbohydrate metabolic pathways to disturbance by endotoxin.
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PMID:Effects of endotoxin on carbohydrate metabolism in inbred mice. 18 6

A girl aged 3 years and 11 months, with recurrent episodes of unexplained metabolic acidosis, hepatomegaly, and fasting hypoglycemia unresponsive to glucagon, showed profound falls in blood glucose levels in response to oral fructose and glycerol challenge. In vitro analysis of her hepatic glycolytic and gluconeogenic enzymes demonstrated absent fructose-1,6-diphosphatase activity. A therapeutic trial of orally given folic acid, 30 mg daily, did not improve her tolerance for fructose and glycerol. Over the next two years she showed improvement in tolerance to fasting, and to fructose and glycerol loading on dietary management.
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PMID:Fructose-1,6-diphosphatase deficiency. 19 69

We treated a two-month-old infant with servere intractable hypoglycemia and nesidioblastosis with continuous glucose infusions (0.75 g per kilogram per hour) via a central venous catheter. Preprandial glucose levels on this regimen were 37+/-2 mg per deciliter (+/-S.E.M.). Basal serum insulin levels were within normal fasting levels for this age group but inappropriately elevated for the blood glucose levels. The beta cells were exquisitely sensitive to infusions of synthetic cyclic somatostatin, with a dose-dependent rise in blood glucose and concomitant suppression of serum insulin levels. There was only minimal suppression of plasma glucagon levels. Single subcutaneous injections of 50 microng of protamine zinc somatostatin raised preprandial blood glucose levels to 83+/-3 mg per deciliter for four to five days although preprandial hormone levels were unchanged. These findings indicate that hypoglycemia of infancy is a hyperinsulin state with abnormal basal regulation of insulin secretion.
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PMID:Hypoglycemia of infancy and nesidioblastosis. Studies with somatostatin. 19 7

A case of hyperinsulinism occuring in a newborn, with a birthweight of 4,050 g, is reported. The hypoglycaemia was refractory to the usual therapy (increase of glucose administration per os, and I.V., corticosteroids, glucagon, diazoxide). At surgery, undertaken at 9 days of age, an adenomatous nodule was removed along with the left part of the pancreas. Death occurred at 18 days, after the child had developed a transitory acidoketosic diabetes and an encephalopathy. Measurement of insulin by radio-immunoassay revealed a strong increase in the ratio insulin/glycaemia, characteristic of nesidioblastoma, as well as a high concentration of insulin in the tumor as compared to normal tissue. On the ultrastructural level, the observed features differed from those seen in children and adults and showed an abnormal overload of dense deposits in the cytoplasm of some histiocytes.
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PMID:[Islet cell adenoma with neonatal onset. Clinical, hormonological and ultrastructural study of a case]. 19 46

Crude mediators from stimulated rabbit peritoneal leukocytes (LEM) engender numerous physiologic alterations in rats, which are similar to those observed during infection. One hour after the intraperitoneal injection of crude LEM, plasma insulin and glucagon concentrations are elevated; at 2 h the hormonal alterations are manifested by a 30% increase in hepatic cyclic adenosine 3',5'-monophosphate (cAMP), glycogen depression, and uptake of 14C-labeled nonmetabolizable amino acid analogues (AA). Plasma hormone concentrations reach maximum levels by 5 h and decline by 24 h. The hepatic concentrations of AA parallel the insulin and glucagon responses and correlate with the inverse of insulin/glucagon molar ratio. In spite of mobilization of hepatic glycogen evident at 5 h, plasma glucose concentrations were transiently depressed. Plasma insulin, glucagon, and hepatic AA concentrations were dose dependent. Plasma insulin and glucagon responses to crude LEM may explain increases in hepatic cAMP, uptake of AA, and glycogenolysis as well as hypoglycemia. These data partially characterize the role of crude LEM, provide an explanation for the stimuli-inducing hyperglucagonemia and hyperinsulinemia during infection. They implicate the endocrine pancreas as a factor regulating the host's metabolic response to infection.
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PMID:Effect of leukocytic endogenous mediators on endocrine pancreas secretory responses. 19 70


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