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)

Hypoglycemia is often associated with typical, but not specific symptoms. A differentiation is made between neuroglucopenic symptoms (e.g., confusion, somnolence) on the one hand, and those that arise as a result of the counterregulatory response of the sympathetic nervous system (e.g., tremor, sweating), on the other. The diagnosis of hypoglycemia can cause considerable problems, in particular when only isolated single symptoms present (e.g., confusion, psychosis, seizures, coma). For the elective clarification of recurrent hypoglycemia, further diagnostic examinations (e.g., fasting with determination of hormones, measurement of insulin) are employed in addition to the patient's history. For differential diagnostic considerations not only organic causes, but also adverse drug reactions and a factitious genesis must be excluded. In the event of an emergency (e.g., hypoglycemic coma) the usual form of treatment is the administration of glucoses or glucagon.
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PMID:[Hypoglycemia. Symptoms, differential diagnosis, therapy]. 917 11

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

The central action of the peptide of intestinal tract, glucagon, was studied in Albino Swiss mice (20-25 g) and Wistar rats (200-220 g). Glucagon was injected intracerebroventricularly (icv) at the dose of 0.25, 0.5 and 1 microgram in 1 microliter of distilled water per mouse or 5 micrograms in 5 microliters per rat. It was found that glucagon administered icv increased glucose content in the peripheral blood serum. Behavioral studies have shown that glucagon diminished spontaneous locomotor activity in rats and mice, impaired exploratory activity and reduced amphetamine-induced hyperactivity. The results were not dependent on hyperglycaemia because the administration of 20% glucose solution po did not cause above effects. In addition, glucagon potentiated cataleptogenic effects of haloperidol. Icv injection of glucagon did not change the pain sensitivity or seizure susceptibility. The substance did not show the anxiolytic properties and did not affect the duration of hexobarbital-induced sleep. In biochemical studies it was found that glucagon injected icv induced the decrease in GABA content while the DA content was increased. The utilization of DA was not changed. The obtained results indicated, that glucagon injected icv exerted the central action, which was manifested by the central regulation of glucose level in the periphery. Moreover, glucagon inhibited the locomotor and exploratory activity as well as the amphetamine-induced hyperactivity and enhanced haloperidol-induced catalepsy. These effect could be connected with the inhibition of the central dopaminergic structures by glucagon.
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PMID:Central action of glucagon. 979 64

Hypoglycaemia is a frequent acute complication of IDDM and is usually defined as a blood glucose level below 3.0 mmol/l. Hypoglycaemia stimulates several neuroendocrine responses, such as secretion of glucagon, adrenaline, growth hormone and cortisol, which are generally increased during this phenomenon. The true prevalence of hypoglycaemia is not known. Studies of the epidemiology of severe hypoglycaemia give prevalences ranging from 2.7 to 85.7 episodes per 100 patients per year. The major risk factor for severe hypoglycaemia is hypoglycaemia unawareness, which occurs particularly in patients with type 1 diabetes of long duration and in those with a history of frequent episodes of hypoglycaemia. The first step in the management of hypoglycaemia is to check blood glucose and to treat hypoglycaemia on the basis of symptoms. Hypoglycaemia requires urgent treatment with a fast-acting carbohydrate or, if severe, with parenteral glucagon or intravenous glucose. Prevention measures should be instituted to prevent subsequent episodes, particularly in younger children with hypoglycaemic seizures or when seizures are recurrent.
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PMID:Hypoglycaemia in children with type 1 diabetes mellitus. 1019 51

A six-year-old, spayed female, cocker spaniel was presented for hypoglycemic seizures. Hypoglycemia with concomitant hyperinsulinemia suggested an insulin-secreting tumor. Pancreatic masses were resected, and insulinoma was diagnosed. Six weeks later, the dog presented in hyperinsulinemic-hypoglycemic crisis (HHC). The dog was initially stabilized with intravenous dextrose boluses and infusions, but seizure activity recurred and persisted. A glucagon constant-rate infusion (GCRI) was initiated, and neurological signs quickly resolved. Dextrose was withdrawn over 24 hours, and euglycemia was maintained by GCRI alone. Despite aggressive medical management including the use of prednisone, diazoxide, bovine somatotropin, and streptozocin, the dog presented on two subsequent occasions in HHC and both times was rapidly stabilized with GCRI alone. In this dog, GCRI was a fast, safe, and effective method of achieving and maintaining euglycemia despite intractable hyperinsulinism. The clinical use of GCRI merits further investigation for management of HHC in veterinary species.
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PMID:Glucagon constant-rate infusion: a novel strategy for the management of hyperinsulinemic-hypoglycemic crisis in the dog. 1066 3

To ascertain if significant hypoglycaemic episodes can be avoided or managed more appropriately in children with insulin dependent diabetes mellitus (IDDM). A retrospective chart audit was performed on all children with IDDM admitted with hypoglycaemia between 1.1.90 and 31.8.97. Of the 21 children studied, 9 presented with seizures and 1 with coma. In 9 the hypoglycaemia was unexplained. Only 6 parents used glucagon. Five children were readmitted during the review with a further hypoglycaemic episode. Four of these had their first admission significantly sooner after diagnosis than those without recurrent episodes. Hypoglycaemic episodes are often unexplained and are unlikely to be completely avoidable. Improved support services during intercurrent illness may reduce the frequency of some hypoglycaemic episodes and increased use of glucagon at home may reduce the severity of some. Children who have their first hypoglycaemic episode within one year of diagnosis are at risk of having recurrent episodes.
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PMID:Hypoglycaemic episodes in children with insulin dependent diabetes mellitus--can the frequency or severity be reduced? 1132 Nov 69

Somatostatin (SRIF, somatotropin release inhibiting factor), discovered for its inhibitory action on growth hormone (GH) secretion from pituitary, is an abundant neuropeptide. Two forms, SRIF14 and SRIF28 exist. Recently, a second family of peptides with very similar sequences and features was described; the cortistatins (CST), CST17 and CST29 which are brain selective. The five cloned SRIF receptors (sst1-5) belong to the G-protein coupled/ heptathelical receptor family. Structural and operational features distinguish two classes of receptors; SRIF1 - sst2/sst3/sst5 (high affinity for octreotide or seglitide) and SRIF2 = sst1/sst4(very low affinitty for the aforementioned ligands). The affinity of SRIF receptors for somatostatins and cortistatins is equally high, and it is not clear whether selective receptors do exist for one or the other of the peptides. Several radiologlands label all SRIF receptors, e.g., [125]LTT-SRIF28' [l25I]CGP23996, [125]Tyr10cortistatin or [125I]Tyr11SRIF14. In contrast, [125I]Tyr3octreotide, [125I]BIM23027, [125I]MK678 or [125I]D-Trp8SRIF14 label predominantly SRIF1 sites, especially sst2 and possibly sst5 receptors. In brain, [125I]Tyr3octreotide binding equates with sst2 receptor mRNA distribution. Native SRIF2receptors can be labeled with [125I]SRIF14 in the presence of high NaCl in brain (sst1) or lung (sst4) tissue. Short cyclic or linear peptide analogs show selectivity for sst2/sst5 (octreotide, lanreotide, BIM 23027), sst1 (CH-275), sst3 (sst3-ODN-8), or sst5 receptors (BIM 23268); although claims for selectivity have not always been confirmed. Beta peptides ith affinity for SRIF receptors are also reported. The general lack of SRIF receptor antagonists is unique for peptide receptors, although CYN 154806 is a selective and potent sst2 antagonist. Nonpeptide ligands are still rare, although a number of molecules have been reported with selectivity and potency for sst1 (L 757,519), sst2 (L 779,976), sst3 (L 796,778), sst4 (NNC 26-9100, L 803,087) or sst1/sst5 receptors (L 817,018). Such molecules are essential to establish the role of SRIF receptors, e.g., sst1 in hypothalamic glutamate currents: sst2 in inhibiting release of GH, glucagon, TSH, gastric acid secretion, pain, seizures and tumor growth, and sst5 in vascular remodeling and inhibition of insulin and GH release.
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PMID:Drug design at peptide receptors: somatostatin receptor ligands. 1193 45

Glucagon-like peptide-1 (GLP-1) is a gut peptide that, together with its receptor, GLP-1R, is expressed in the brain. Here we show that intracerebroventricular (i.c.v.) GLP-1 and [Ser(2)]exendin(1-9) (HSEGTFTSD; homologous to a conserved domain in the glucagon/GLP-1 family) enhance associative and spatial learning through GLP-1R. [Ser(2)]exendin(1-9), but not GLP-1, is also active when administered peripherally. GLP-1R-deficient mice have a phenotype characterized by a learning deficit that is restored after hippocampal Glp1r gene transfer. In addition, rats overexpressing GLP-1R in the hippocampus show improved learning and memory. GLP-1R-deficient mice also have enhanced seizure severity and neuronal injury after kainate administration, with an intermediate phenotype in heterozygotes and phenotypic correction after Glp1r gene transfer in hippocampal somatic cells. Systemic administration of [Ser(2)]exendin(1-9) in wild-type animals prevents kainate-induced apoptosis of hippocampal neurons. Brain GLP-1R represents a promising new target for both cognitive-enhancing and neuroprotective agents.
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PMID:Glucagon-like peptide-1 receptor is involved in learning and neuroprotection. 1294 21

OBJECTIVE: To report a case of Persistent Hyperinsulinemic Hypoglycemia in twins which is a situation not yet reported in the literature. METHODS: Report of seizures in identical twins, from consanguineous parents, with persistent hypoglycemia as cause of the seizures. Laboratory tests, performed for etiological investigation of the hypoglycemia, included thyroid hormones (T4/TSH), insulin, cortisol, growth hormone, stimulation test with glucagon (to evaluate the insulin/glucose relation), and histopathological study of the pancreas. RESULTS: Laboratorial investigation revealed a persistent hypoglycemia with hyperinsulinism which were confirmed with the stimulation test with glucagon. The histopathological exam showed a persistence of first generation pancreatic islet, confirming the diagnosis of Persistent Hyperinsulinemic Hypoglycemia in Infancy (the new denomination of Nesidioblastosis). CONCLUSION: Although rare, this condition must be early suspected early in the evaluation of hypoglycemia of the young infant, even out of the neonatal period, specially if the parents are consanguineous. The adequate therapy must be quickly initiated in order to prevent neurological damage.
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PMID:[Persistent hyperinsulinemic hypoglycemia of infancy: case report] 1464 92


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