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)

We studied 20 children with a clinical picture and laboratory study suggestive of hepatic glycogenosis. The age of the beginning of symptoms varied from birth to 24 months and the age at the diagnosis varied from 2 to 81 months. Hepatomegaly was found in all patients, diarrhea in 65% (13/26), "doll-face" in 55% (11/20) and convulsions in 50% (10/20). Nutritional evaluation showed more height deficiency than weight deficiency. Laboratory tests showed elevation of hepatic transaminases (12/19), hypercolesterolemia (8/14), hyperuricemia (6/17) and hypoglycemia (6/20). Liver function was not compromised in most of the cases. The results of glucagon tolerance test were variable. The histoenzymology study performed in 15 patients revealed the following results: Type VI (liver phosphorylase deficiency) in seven, Type I (glucose-6-phosphatase deficiency) in two, Type IV (brancher enzyme) in one and no conclusion could be drawn in five patients. The finding of hypoglycemia in few cases of this study can be justified by the few number of glycogenosis Type I, probably due to the fact that this type is the most easily diagnosed, with less necessity of referring them to specialized centers.
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PMID:[Hepatic glycogenosis in childhood: clinical and laboratory findings in 20 patients]. 872 90

ANP increases insulin levels in vivo. Because in vitro an ANP-induced increase in cGMP levels of islets of Langerhans was observed but no simultaneous increase in insulin release, secreted glucagon may be a candidate for this second messenger affected by ANP. The inhibitory effect of glucose on glucagon secretion was pronounced by 1.0 nM ANP at 3.0 mM glucose as well as at 5.6 and 8.3 mM glucose. Because in other tissues cGMP (the specific second messenger of ANP1 inhibits Ca2+ channels, the uptake of 45Ca2+ was investigated. ANP (1.0 nM) inhibited 45Ca2+ uptake, which was nearly completely abolished by a pertussis toxin (PT) pretreatment. The inhibition of 45Ca2+ uptake fits to inhibitory ANP effects on glucagon secretion but does not fit to insulin secretion. The glucagon secretion coupling cascade affected by ANP probably involves an increase in cGMP because 8-Br-cGMP (a membrane-permeable cGMP analogue) also decreased glucagon secretion. ANP(4-23), a truncated form of ANP, which is selective for the ANP clearance receptor, also inhibited glucagon secretion. HS-42-1, a guanylate cyclase receptor antagonist, tended to reverse the effect of ANP on glucagon release. The data indicate that in the presence of ANP, the in vivo homeostasis of glucose, though plasma insulin levels are increased, is not due to an ANP-mediated increase in glucagon secretion; ANP has a complex inhibitory effect on glucagon release. The data further indicate that the ANP-induced inhibition of glucagon secretion probably involves the cGMP system, an inhibition of Ca2+ uptake and the involvement of PT-sensitive G-proteins. Moreover, an involvement of the clearance receptor seems to be likely. ANP is a valuable tool for investigating glucagon secretion from pancreatic islets because paracrine effects of insulin can be excluded.
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PMID:Atrial natriuretic peptide (ANP)-induced inhibition of glucagon secretion: mechanism of action in isolated rat pancreatic islets. 889 23

The central action of periplanetin CC-1 (Pea-HrTH) (Glp-Val-Asn-Phe-Ser-Pro-Asn-TrpNH2), octapeptide of the insect adipokinetic hormone family (AKH-family), isolated from American cockroach-Periplaneta americana, was studied in Albino Swiss mice (20-25 g). CC-1 was injected intracerebroventricularly (i.c.v.) in the volume of 5 microliters at the dose of 50 ng/mouse. It was found that CC-1 showed strong analgesic activity in "writhing syndrome" test and in "hot plate" test. In addition, periplanetin CC-1 decreased the threshold for tonic seizures and increased mortality in pentetrazole-induced seizures, having no influence on the electric convulsions. CC-1 is known to be a glucagon-like AKH in insects. However, administered i.c.v. to mice, it did not increase the peripheral blood glucose level. The obtained results indicate that periplanetin CC-1 shows a biological action in vertebrates, but its metabolic effects are different than in insects.
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PMID:Central action of insect neuropeptide, periplanetin CC-1, in mice. 943 51

Glucose infusion can prevent the increase in glucose production (Ra) and increase glucose uptake (Rd) during exercise of moderate intensity. We postulated that 1) because in postabsorptive intense exercise (>80% maximal O2 uptake) the eightfold increase in Ra may be mediated by catecholamines rather than by glucagon and insulin, exogenous glucose infusion would not prevent the Ra increment, and 2) such infusion would cause greater Rd. Fit young men were exercised at >85% maximal O2 uptake for 14 min in the postabsorptive state [controls (Con), n = 12] or at minute 210 of a 285-min glucose infusion. In seven subjects, the infusion was constant (CI; 4 mg . kg-1 . min-1), and in seven subjects it was varied (VI) to mimic the exercise Ra response in Con. Although glucose suppressed Ra to zero (with glycemia approximately 6 mM and insulin approximately 150 pM), an endogenous Ra response to exercise occurred, to peak increments two-thirds those in Con, in both CI and VI. Glucagon was unchanged, and very small increases in the glucagon-to-insulin ratio occurred in all three groups. Catecholamine responses were similar in all three groups, and correlation coefficients of Ra with plasma norepinephrine and epinephrine were significant in all. In all CI and VI, Rd at rest was 2x Con, increased earlier in exercise, and was higher for the 1 h of recovery with glucose infusion. Thus the Ra response was only partly attenuated, and the catecholamines are likely to be the regulators. This suggests that an acute endogenous Ra rise is possible even in the postprandial state. Furthermore, the fact that more circulating glucose is used by muscle during exercise and early recovery suggests that muscle glycogen is spared.
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PMID:Glucose infusion partially attenuates glucose production and increases uptake during intense exercise. 968 28

This report details the management of a newborn with nesidioblastosis who underwent a 95% pancreatectomy under general anaesthesia. The baby presented with hypoglycemic convulsions, due to hyperinsulinism, and was treated with 12.5% dextrose infusions, glucagon and anticonvulsants. Intraoperatively and postoperatively the baby remained hyperglycemic. A postoperative osmotic diuresis necessitated the use of insulin for brief period. The infant remained euglycemic and convulsion free, following discontinuation of the dextrose infusions and starting of oral feeds. Recovery was uneventful.
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PMID:Anaesthetic management of nesidioblastosis in a newborn. 971 92

Excessive body building may be dangerous. To promote athletic performance and to improve physical appearance many of the body builders abuse anabolic-androgenic steroids and other drugs. The abuse of insulin as an anabolic medication in this athletic community was followed by a case of severe hypoglycaemia in a body builder. A 30-year old male presented with cerebral symptoms of hypoglycaemia. Directly before an international competition he tried to stimulate muscle growth by using the hypoglycaemic stimulus to the growth hormone. To achieve this he injected 70 IE of a short-acting insulin subcutaneously, resulting in severe hypoglycaemia. After the initial administration of intravenous glucose by the paramedics, he lost consciousness and showed signs of convulsions. After orotracheal intubation by an emergency physician, despite of ongoing infusion of glucose the blood glucose concentration remained low as measured in the out-of-hospital setting. Finally administration of additional glucose and glucagon in the intensive care unit was able to stabilize the metabolic system. In any case of severe hypoglycaemia, repetitive measurements of blood glucose even in the prehospital setting should be performed to detect the hypoglycaemia especially if athletes are concerned.
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PMID:[Insulin as an anabolic: hypoglycemia in the bodybuilding world]. 972 65

Previous studies in avian species have reported time-dependent losses in muscle glycogen with prolonged feed withdrawal (FW). However, cervical dislocation was used to collect tissues, a method that results in significant involuntary muscle convulsions. In this study, cervical dislocation alone was found to reduce muscle glycogen by 23%, therefore, barbiturate overdose was used to collect tissue samples before and after FW, at the end of refeeding, and from continuously fed controls at each interval. Additionally, plasma samples from 6-wk-old male chickens were taken at the initiation and end of a 24-hr feed withdrawal, and at various times during refeeding. After 24 hr of FW, liver glycogen decreased markedly (77%; P < 0.05), whereas muscle glycogen decreased slightly and transiently, such that it returned to and remained at control levels, even after prolonged (72 hr) FW. Plasma glucose was decreased, whereas glucagon was elevated after a 24-hr feed withdrawal (P < 0.05), when compared with control concentrations. Muscle glycogen levels were not significantly increased over control levels after refeeding, but liver glycogen was increased by 380% (P < 0.05). Feed deprivation followed by refeeding resulted in increased circulating insulin and glucose levels when compared with control levels. Therefore, by using methods of tissue collection that ensure that muscle glycogen determinations are not confounded by artifactual degradation, these results verify that regulation of avian muscle glycogen stores is similar to that in mammals.
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PMID:Relative insensitivity of avian skeletal muscle glycogen to nutritive status. 1037 Aug 63

We report on a 35-week gestation infant who developed severe hyponatremia and thrombocytopenia after continuous infusion of glucagon for the treatment of intractable hypoglycemia. Given these serious side effects,glucagon infusion should be avoided in the treatment of premature infants.hypoglycemia, glucose, small for gestational age. Hypoglycemia is commonly seen in premature infants, and the provision of a standard glucose intake is often not sufficient to maintain euglycemia. For these infants, an increase in glucose infusion to provide 4 to 8 mg/kg/min is initially recommended.1 Should this approach fail, pharmacologic agents such as corticosteroids or diazoxide are indicated.1 When the serum glucose in premature or small for gestational age infants cannot be adequately maintained, a glucagon infusion is now suggested as the best treatment approach.2,3 We report the use of glucagon infusion for the treatment of severe hypoglycemia in a premature infant. A severe hyponatremia associated with transient convulsions and thrombocytopenia was observed in the neonate after treatment. Discontinuation of the glucagon infusion resulted in prompt resolution of these abnormalities.
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PMID:Continuous infusion of glucagon induces severe hyponatremia and thrombocytopenia in a premature neonate. 1250 83

Four cases of asthma (one adult, three children) developing acute adrenal crisis after introduction of high-dose inhaled fluticasone proprionate are presented. The three children, aged 7-9 yrs, had been prescribed inhaled fluticasone, dosage 500-2,000 microg x day(-1) and duration 5 months-5 yrs. All presented with convulsions due to hypoglycaemia (blood glucose 1.3-1.8 mM). The fourth case was a male of 33 yrs with difficult-to-control asthma and had been taking fluticasone propionate 1,000-2,000 microg x day(-1) for 3 yrs. He presented with fatigue, lethargy, nausea and postural hypotension. Acute adrenal crisis in each case was confirmed by investigations which included measurement of acute phase cortisol levels, short and long Synacthen stimulation tests and glucagon stimulation tests. Other cases of hypthoalamic-pituitary-adrenal axis suppression were excluded.
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PMID:Acute adrenal crisis in asthmatics treated with high-dose fluticasone propionate. 1210 82

Hyperinsulinism, although rare, is the most common cause of persistent hyperinsulinaemic hypoglycaemia in infancy. Because of persistent hypoglycaemia, serious difficulties are encountered in the long term management of this condition. A male neonate, after an uncomplicated full-term pregnancy, had been admitted to another hospital with convulsions on the third post-natal day. Meningitis had been suspected at that time and treated with phenobarbital and he had been discharged from the hospital. At three-months old he was referred to our department for persistent convulsions and lethargy. His parents were of 1st degree consanguinity. His blood glucose level was found to be 24 mg/dl (1.33 mmol/L). Because of the dangerously high insulin level during hypoglycaemia (insulin/glucose > 0.3), the absence of ketonuria, and the need for a high dose of glucose infusion (> 15 mg/kg/min) to achieve normoglycaemia and a glycaemic response to glucagon despite the hypoglycaemia, a diagnosis of persistent hyperinsulinaemic hypoglycaemia of infancy was made. Since maximal doses of prednisone, glucagon, diazoxide, octreotide and high infusion of glucose were ineffective in achieving normoglycaemia, a subtotal (80%) pancreatectomy was done. Postoperatively intermittent hypoglycaemic episodes continued. These were controlled with low doses of octreotide. Histology revealed diffuse adenomatous hyperplasia (nesidoblastosis). The boy is now in the sixth post-operative month and developing normally.
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PMID:Persistent hyperinsulinaemic hypoglycaemia of infancy: case report. 1263 64


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