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)

Recent advances in the field of peptide chemistry and gene technology have resulted in an explosive accumulation of information on the chemical structures of gastrointestinal hormones. Based on the information, chemical syntheses of these peptides or their shorter fragments and analogs have been performed. Synthetic peptides related to the hormones have now become important tools in searching for functions of peptides and in producing region-specific antisera to the respective peptides. Using these antisera, hormone-producing cells were clearly identified and the post-translational biosynthetic processings in the cells were demonstrated. Recent immunohistochemical studies have also revealed that cells contain and can release a variety of peptides or amines that are capable of influencing target cells and acting as hormone, neurotransmitter or neuromodulator. In addition, recent studies on galanin and glucagon-like peptide-1 (GLP-1) are described.
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PMID:[Recent advances in gastrointestinal hormones]. 170 1

The neuropeptide galanin has been identified as a potential sympathetic cotransmitter in the canine pancreas. Immunoreactive galanin, also present in nerve fibers of the pig pancreas, was therefore measured in the effluent from isolated perfused pig pancreas with preserved sympathetic (splanchnic) or parasympathetic (vagal) innervation with radioimmunoassays directed against both the N-terminus and the C-terminus of galanin. Electrical vagus stimulation increased the pancreatic exocrine secretion, the secretion of insulin and glucagon, and the release of VIP, but did not influence galanin release. Splanchnic nerve stimulation increased perfusion pressure and glucagon secretion, inhibited insulin secretion, and increased the release of NPY, but galanin release was not affected. We conclude that the pancreatic galanin nerve fibers belong neither to the sympathetic nor to the parasympathetic divisions of the efferent nerve supply to the pig pancreas.
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PMID:Neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP), but not galanin, are autonomic cotransmitters in the porcine pancreas. 172 Oct 82

Food intake can be increased or decreased after either central or peripheral administration of peptides. Galanin, neuropeptide Y, opioid peptides, growth-hormone-releasing hormone, and desacetyl-melanocyte stimulating hormone increase food intake whereas insulin, glucagon, cholecystokinin, anorectin, corticotropin-releasing hormone, neurotensin, bombesin, cyclo-his-pro, and thyrotropin-releasing hormone reduce food intake. Many of these peptides have reciprocal effects on food intake and sympathetic activity with those peptides that stimulate food intake reducing sympathetic activity and vice versa. In addition, neuropeptide Y specifically increases carbohydrate intake. Galanin and opioid peptides on the other hand increase fat intake whereas enterostatin reduces fat intake. Glucagon decreases protein intake. The effect of peptides on specific nutrients suggests that peptides may work in part by modulating basic feeding mechanisms to lead to the selection of specific nutrients from the diet. This hypothesis might be called a nutrient-specific model of peptide-induced food intake.
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PMID:Peptides affect the intake of specific nutrients and the sympathetic nervous system. 172 38

Galanin, an ubiquitous neuropeptide, was recently shown to inhibit somatostatin release by the rat islet tumor cell line, Rin-m. By using the clonal pancreatic delta cell line Rin14B, originating from Rin-m cells, we were able to identify the presence of one type of specific galanin-binding site of high affinity (Kd = 1.6 nM; maximal binding capacity = 270 fmol/mg protein) and high specificity for the peptide. Binding of 125I-galanin to these receptors was time-dependent and highly sensitive to guanine nucleotides. Using the cross-linker disuccinimidyl tartrate, covalent linking of the galanin receptor to 125I-galanin in membranes from Rin14B cells, followed by SDS/PAGE analysis of membrane proteins, indicated that the galanin receptor is a protein of 54 kDa. 0.1-100 nM galanin also exerted a marked inhibitory effect on the cAMP-production system under basal conditions, as well as in the presence of the pancreatic peptide glucagon. At a maximal dose, galanin induces a 90-100% decrease of basal and glucagon-stimulated cAMP production levels, with a median inhibition concentration (IC50) of 3 nM galanin. The direct inhibitory effect of galanin on the adenylate cyclase activity in Rin14B cell membranes was also demonstrated (IC50 = 3 nM galanin). The inhibitory effect of galanin on the basal and glucagon-stimulated cAMP production in Rin14B cells was reversed by pertussis toxin. The toxin was also shown to specifically ADP-ribosylate a protein of 41 kDa in membranes from Rin14B cells. Taken together, these data show that the pancreatic delta cell line Rin14B expresses high affinity galanin receptors negatively coupled to a pertussis-toxin-sensitive cAMP-production system.
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PMID:A clonal rat pancreatic delta cell line (Rin14B) expresses a high number of galanin receptors negatively coupled to a pertussis-toxin-sensitive cAMP-production pathway. 184 83

It is clear that the sympathoadrenal system has a role in the regulation of endocrine pancreatic function and that the sympathetic nerves of the pancreas can change pancreatic hormone secretion to increase the availability of metabolic fuels. It seems likely that the classical sympathetic neurotransmitter, NE, acts in concert with peptide co-transmitters, such as galanin and NPY. Each is released during the stimulation of pancreatic sympathetic nerves and each is capable of influencing either islet function or pancreatic blood flow. There is considerable indirect evidence that the sympathetic innervation of the pancreas is activated during acute stress and influences the endocrine pancreas. However, proving such a physiologic role is difficult because of redundant mechanisms that influence the secretion of the metabolically-crucial hormones, insulin and glucagon. Such definitive proof therefore awaits the development of new techniques to dissect and dissociate these mechanisms.
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PMID:Neural control of islet function by norepinephrine and sympathetic neuropeptides. 192 79

Synthetic galanin, infused at a rate of 4 micrograms/kg body weight/h for 30 min, elicited a mild but significant hyperglycemia in conscious dogs and a fall in plasma insulin. Pancreatic glucagon, epinephrine, norepinephrine, cortisol and growth hormone levels were not affected significantly. The mild hyperglycemic action of galanin seems to be due to an inhibition of insulin production. Thus galanin appears to be involved in glucose homeostasis.
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PMID:Galanin-induced hyperglycemia: effect on insulin and glucagon. 242 25

Galanin, a 29-aminoacid neuropeptide, was infused for 60 min into healthy volunteers at 7.8 pmol/kg/min (n = 4) or 33.2 pmol/kg/min (n = 6). During the infusion there was no change in heart rate or blood pressure and the only symptoms were a transitory bitter taste and slight hypersalivation. Plasma growth hormone levels rose during the high-dose galanin infusion from 2.8 +/- 0.8 mU/l to a mean peak of 48.5 +/- 19.8 mU/l; prolactin levels rose from 176 +/- 33 mU/l to 274 +/- 33 mU/l. A significant rise in growth hormone also occurred with the low-dose infusion (2.5 +/- 1.1 mU/l to a mean peak of 23.5 +/- 6.6 mU/l). There was no change in cortisol, thyroid-stimulating hormone, follicle-stimulating hormone, or luteinising hormone at either dose. 20 min after the start of the infusion a 25 g glucose bolus was given intravenously. Galanin reduced glucose clearance without significantly affecting plasma insulin concentrations. Pancreatic polypeptide levels were suppressed by the galanin infusion but levels of glucagon and gastric inhibitory peptide were unchanged.
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PMID:Growth hormone release in man induced by galanin, a new hypothalamic peptide. 242 4

Immunofluorescent staining for galanin in canine pancreatic tissue was performed together with an evaluation of the effects of synthetic galanin on pancreatic output of glucagon, somatostatin, and insulin in pentobarbital-anesthetized dogs. A dense network of galaninlike immunoreactive nerve fibers was visualized in association with the islets of Langerhans and occasional galanin immunoreactive fibers were seen to course through the exocrine parenchyma of dog pancreas. During intravenous infusion of synthetic porcine galanin (25 pmol X kg-1 X min-1) pancreatic glucagon output rapidly doubled, and the output of both somatostatin and insulin decreased by 70%. Because arterial and pancreatic venous catecholamine levels remained unchanged, the effects on hormone secretion were not secondary to activation of the sympathetic nervous system. The direct pancreatic action of galanin was confirmed by infusing a peripherally ineffective dose of galanin (0.25 pmol X kg-1 X min-1) into the pancreatic artery, which also stimulated glucagon (+90%) and suppressed somatostatin (-50%) and insulin (-70%) release. The presence of galaninlike immunoreactive neurons in dog islets, together with the direct action of galanin on pancreatic hormone release, suggest that this recently discovered peptide could serve as an important neuromodulator of endocrine pancreatic function.
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PMID:Galanin: a novel pancreatic neuropeptide. 242 33

Intravenous infusion of galanin into conscious dogs during ingestion of oral glucose or a mixed meal or during iv infusion of arginine resulted in significant blunting of plasma insulin responses and significant increases in plasma glucose levels compared to those in control experiments. Galanin infusions did not significantly alter plasma gastric inhibitory peptide responses to oral glucose or a mixed meal, or plasma gastrin, pancreatic polypeptide, or pancreatic glucagon responses to a mixed meal. Similarly, galanin infusions did not significantly alter pancreatic glucagon responses to iv arginine. In all experimental situations, on cessation of the galanin infusions, prompt elevation of plasma insulin levels occurred. These results suggest that in the conscious dog, galanin administration produces a relatively selective, but readily reversible, inhibition of insulin secretion stimulated by oral nutrients or iv arginine.
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PMID:The effect of galanin on canine plasma glucose and gastroenteropancreatic hormone responses to oral nutrients and intravenous arginine. 242 32

Galanin was recently demonstrated to be a neuropeptide in intrapancreatic nerves. In this study, the effects of galanin on basal and stimulated insulin and glucagon secretion in the mouse were investigated. Galanin, injected intravenously at dose levels ranging from 0.53 to 8.5 nmol kg-1, markedly lowered basal plasma insulin levels and transiently increased basal plasma glucagon levels. Furthermore, galanin induced hyperglycaemia: plasma glucose levels were 11 +/- 0.2 mmol l-1 2 min after injection of galanin (4.25 nmol kg-1) compared with 9.3 +/- 0.3 mmol-1 in controls (P less than 0.001). Galanin also impaired the plasma insulin response to either glucose or the cholinergic agonist carbachol. Thus, galanin (4.25 nmol kg-1) inhibited the plasma insulin response to glucose by 65% (P less than 0.001), and that to carbachol by 85% (P less than 0.001). Moreover, glucose abolished the galanin-induced plasma glucagon response. Also, galanin and carbachol exerted additive stimulatory effects on glucagon levels. It is concluded from this study in mice that galanin inhibits basal and stimulated insulin secretion, stimulates glucagon secretion, and induces hyperglycaemia. It is suggested that the intrapancreatic neuropeptide galanin is of importance in the regulation of both insulin and glucagon secretion.
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PMID:Galanin: effects on basal and stimulated insulin and glucagon secretion in the mouse. 243 68


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