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)

In rats, total gastrectomy (TG) has been shown to induce pancreatic hyperplasia and increased tissue concentrations of pancreatic trypsin and amylase, whereas lipase concentration was decreased. We performed total gastrectomy with the additional insertion of a duodenal tube in 17 rats. A central venous catheter was placed after 3 wk. The control groups consisted of sham-operated rats with a gastrotomy plus duodenal tube and a group of rats with only a duodenal tube. The rats received meal stimulation with a 6 mL liquid diet (3 mL oil, 2 mL amino acid solution, and 1 mL glucose) via duodenal tube upon recuperation. Blood samples were taken before as well as 5, 15, 30, and 60 minutes after the meal and analyzed for insulin, pancreatic glucagon, gastrin, and CCK by specific RIA techniques. Glucose tolerance was found to be impaired after total gastrectomy. Though insulin release was delayed compared to the controls, the integrated postprandial output was unchanged. The pancreatic glucagon release after the meal increased 83% in TG rats, compared to control rats. The baseline and postprandial gastrin values diminished 70% compared to control animals. Neither group exhibited a postprandial increase in gastrin levels. TG led to an increased postprandial CCK output of 72% compared to controls. The trophic changes of rat exocrine pancreas following total gastrectomy, therefore, could be based on an elevated postprandial release of CCK.
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PMID:Cholecystokinin influences pancreatic trophism following total gastrectomy in rats. 266 36

Cholecystokinin octapeptide (CCK-8) and glucagon (GLG) decrease food intake of a number of species. However, the responsiveness of rats to the food intake effects of these peptides may develop differentially due to sex, age and/or developmental state. Male and female weanling rats decreased early dark cycle food intake following the administration of 5 and 10 micrograms/kg CCK-8 and male rats were more responsive than female rats, p less than 0.05. GLG did not decrease early dark cycle food intake of either male or female weanling rats. Weanling male rats increased plasma glucose and insulin levels in response to GLG administration, p less than 0.05. Male rats were retested with GLG (250 and 500 micrograms/kg) at 6, 9 and 22 weeks of age. GLG did not decrease food intake of these rats until they reached 9 weeks of age and they were still responsive at 22 weeks of age, p less than 0.05.
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PMID:The effect of cholecystokinin octapeptide and glucagon (1-29) on food intake of weanling rats. 267 41

The effects of intracerebroventricular (icv) vasoactive intestinal polypeptide (VIP), secretin, glucagon, and cholecystokinin-octapeptide (CCK-8) on the thermoregulatory and cardiovascular systems were studied in conscious rats. The icv injection of VIP at a dose of 10 micrograms produced hyperthermia with an increase in the positive difference between the interscapular brown adipose tissue (BAT) and colonic temperatures (TBAT-Tco), but had little effect on nonevaporative heat loss. Mean arterial blood pressure and heart rate increased following the icv VIP. The results were consistent at ambient temperatures (Ta) of 18, 23, and 28 degrees C. The icv injection of secretin at doses of 1 and 10 micrograms at Ta of 23 degrees C produced hypothermia with a decrease in (TBAT-Tco) and elevated blood pressure without any change in heart rate. The 10 micrograms of icv glucagon had no effect on the thermoregulatory and cardiovascular systems. The large dose of icv CCK-8 (10 micrograms) induced persistent hyperthermia. Nonsulfated-form CCK-8 and CCK-tetrapeptide, however, were ineffective on all variables measured. These results indicate that the central VIP activates BAT thermogenesis and induces hyperthermia, but has a minimum effect on nonevaporative heat loss. Although VIP, secretin, and glucagon have similarities in terms of chemical structure, their effects on body temperature, BAT thermogenesis, and the cardiovascular system are quite different.
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PMID:Changes in brown adipose tissue metabolism following intraventricular vasoactive intestinal peptide and other gastrointestinal peptides in rats. 279 18

Protein- and fat-rich test meals elicit a strong stimulatory effect on postprandial somatostatin (SLI) and pancreatic polypeptide (PP) release, whereas carbohydrate-rich meals rather attenuate the response of both hormones. Since there is evidence that intestinal hormones might contribute to the postprandial SLI and PP response, it was the aim of the present study to determine in dogs the effect of low-dose cholecystokinin octapeptide (CCK-8) on basal hormone levels and also during a background infusion of amino acids or glucose. In a group of six conscious dogs, sulfated CCK-8 was infused intravenously (i.v.) via a hindleg vein at stepwise increasing infusion rates of 10, 30, and 50 pmol X kg-1 X h. The infusion of CCK was applied during a background infusion of saline (2 ml/min), glucose (0.2 g/min), or an amino acid mixture (8.5%, 2 ml/min). CCK-8 had no effect on plasma insulin and glucagon levels under all experimental conditions. Plasma SLI levels were significantly stimulated by all doses of CCK. This stimulatory effect was similar during background infusions of either saline, glucose, or amino acids, respectively. Pancreatic polypeptide (PP) levels rose 200-300 pg/ml during CCK plus saline. This was slightly attenuated by glucose. During CCK plus amino acids, the PP response was augmented to 600-800 pg/ml. Since secretin is also released after the ingestion of a meal and intraduodenal acidification is a potent stimulus not only of secretin but also of gastric and pancreatic SLI release, the effect of secretin was examined additionally.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulatory effect of glucose, amino acids, and secretin on CCK-8-induced somatostatin and pancreatic polypeptide release in dogs. 286 95

A large number of antisera mainly raised against mammalian hormones are tested immunocytochemically on the GEP-endocrine system of mouse and fish (Barbus conchonius). The endocrine pancreas of mouse and fish appeared to contain the same four endocrine cell types; insulin-, glucagon-, PP- and somatostatin-immunoreactive cells. In mouse about 13 GEP endocrine cell types are distinguished: 1. insulin-, 2. somatostatin-, 3. glucagon-, 4. PP-, 5. (entero)glucagon-/PP-like, 6. CCK-like, 7. substance P-, 8. neurotensin-, 9. VIP-, 10. gastrin-, 11. secretin-, 12. beta-endorphin-, 13. serotonin-immunoreactive cells. Based on this and a previous study at least 13 GEP endocrine cell types seems to be present in stomachless fish: 1-9 as described for mouse, 10. (entero)glucagon-like, 11. met-enkephalin, 12. VIP-like, 13. unspecific immunoreactive endocrine cells. Coexistence of glucagon and PP-like peptides is found in the gut and pancreas of mice and in the gut of B. conchonius. In mouse pancreas and fish gut, endocrine cells showing only PP- or glucagon-like immunoreactivity are found too. In mouse stomach some endocrine cells showing only PP-immunoreactivity are demonstrated. In the same region coexistence of C-t-gastrin- and FMRF-amide-immunoreactivity is found in endocrine cells. The importance of these phenomena are discussed. Enteric nerves immunoreactive with antisera raised against substance P and GRP are found in mouse, against somatostatin and met-enkephalin in both mouse and fish and against VIP in fish.
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PMID:Immunocytochemical identification and localization of peptide hormones in the gastro-entero-pancreatic (GEP) endocrine system of the mouse and a stomachless fish, Barbus conchonius. 287 13

Calcitonin gene-related peptide (CGRP) exists in nerves throughout the gastrointestinal tract and pancreas, and exogenous CGRP has been reported to inhibit many endocrine and exocrine secretions of the gut and pancreas. Because somatostatin also has widespread inhibitory actions and because both gut and pancreatic somatostatin secretion may be under peptidergic control, we examined the influence of CGRP on circulating levels of somatostatin-like immunoreactivity (SLI) and on hormone output from the duodenal lobe of the dog pancreas in situ. Intravenous infusion of human CGRP in anesthetized dogs increased arterial SLI in a dose-dependent manner. During iv infusion of CGRP at 500 pmol/min, the increment of circulating SLI (change at 20 min, +175 +/- 24 fmol/ml) was composed of nearly equimolar amounts of SLI-14 and SLI-28, suggesting an effect of CGRP on both gastric and intestinal somatostatin secretion. The effect of iv CGRP (500 pmol/min) on arterial SLI exceeded those of iv CCK-8 (440 pmol/min), iv isoproterenol (10 nmol/min), and intragastric administration of acidified liver extract. In contrast, salmon calcitonin (500 pmol/min, iv) was without effect. CGRP did not stimulate pancreatic SLI output when infused iv (500 pmol/min) or when infused directly into a pancreatic artery (5 pmol/min). The pancreatic infusion of CGRP decreased insulin output slightly (change at 20 min, -21 +/- 8%), but did not affect glucagon output. We conclude that CGRP is a most effective yet selective stimulator of gastrointestinal somatostatin release, with little influence on islet function. We suggest that exogenous and possibly endogenous neuronal CGRP could exert inhibitory effects on gastrointestinal function via the release of somatostatin.
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PMID:Calcitonin gene-related peptide: a potent and selective stimulator of gastrointestinal somatostatin secretion. 288 97

The gastro-entero-pancreatic (GEP) endocrine system of a stomach-containing and of a stomachless teleost, Sparus auratus and Barbus conchonius, respectively, are studied immunocytochemically using different antisera against mammalian hormones. Insulin-, glucagon-, somatostatin-, and pancreatic polypeptide (PP)-immunoreactive cells are identified in the endocrine pancreas of both species. Only the distribution of PP-immunoreactive cells differed strongly; in the principal islet of both fishes, few PP-immunoreactive cells are present, whereas in the smaller ones many of them are observed in S. auratus and none in B. conchonius. In the digestive tract of S. auratus 10 endocrine cell types can be distinguished: neurotensin-, secretin-, serotonin-, somatostatin-, and two types of substance P-immunoreactive cells exclusively in the stomach, and C-t-gastrin/CCK-, glucagon-, Met-enkephalin-, PP-, and only one type of substance P-immunoreactive cells in the intestinal epithelium. With the exception of substance P-immunoreactive cells, the other four intestinal endocrine cells, as well as an unspecific immunoreactive cell, can also be found in B. conchonius. Coexistence of glucagon- and PP-like immunoreactivity is observed in the pancreas of S. auratus and in the gut of B. conchonius. Pancreatic and gut endocrine cells showing only PP- or glucagon-like immunoreactivity are found, too.
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PMID:A comparative immunocytochemical study of the gastro-entero-pancreatic (GEP) endocrine system in a stomachless and a stomach-containing teleost. 288 63

The effects of activation of the alpha-adrenoceptors on glucagon secretion are not yet clear. We therefore injected the alpha 1-selective agonist phenylephrine and the alpha 2-selective agonist clonidine (0.05-50 nmol/kg) intravenously to mice and measured the plasma glucagon levels. We found that both phenylephrine and clonidine enhanced the plasma glucagon levels. The peak level of plasma glucagon was seen at 2 min after clonidine injection whereas phenylephrine enhanced the plasma glucagon levels throughout a 10 min period after the injection. Furthermore, both clonidine and phenylephrine potentiated the plasma glucagon response to the cholinergic agonist carbachol and exerted additive stimulatory effects on the plasma glucagon response to both the beta-adrenoceptor agonist terbutaline and the C-terminal octapeptide of cholecystokinin, CCK-8. The elevated plasma insulin levels after injection of carbachol or terbutaline were lowered by clonidine but not by phenylephrine whereas the CCK-8-induced increase in plasma insulin levels was not affected by either clonidine or phenylephrine. We conclude that both alpha 1- and alpha 2-adrenoceptor activation enhances plasma glucagon levels in the mouse, and that alpha 2- but not alpha 1-adrenoceptor activation lowers plasma insulin levels.
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PMID:Alpha 1- and alpha 2-adrenoceptor activation increases plasma glucagon levels in the mouse. 289 47

The endocrine pancreas of Vipera aspis and Natrix maura has been investigated by immunocytochemistry for the presence of six peptides reported to occur in Mammals or in Reptiles. Gastrin/CCK and PP were absent in the endocrine cells, VIP was located within nerve terminals only. Insulin, Glucagon, and Somatostatin were localized both in Vipera and Natrix, generally with a ring of D (Somatostatin) cells surrounding a core of Glucagon (A) and Insulin (B) producing cells; however frequent clusters of D cells are intermingled with the other endocrine cells. Statistical evaluations on the percentages of these 3 cell types showed preponderance of A cells in Natrix whereas in Vipera no significant difference was found between the number of A and B cells. The D cells showed a uniform distribution in the pancreas of the 2 studied species, in any case with a percentage slightly inferior to those of B cells.
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PMID:Immunocytochemical localization of peptides in the endocrine pancreas of the snakes Vipera aspis and Natrix maura. 290 96

This study examined the effects of transmural nerve stimulation, acetylcholine, adrenoceptor agonists and several peptides on the contractility of strips of human gallbladder in vitro. Acetylcholine caused concentration-related contractions of the tissues and the sensitivity to acetylcholine was similar in gallbladders with mild and severe chronic cholecystitis. Noradrenaline and adrenaline relaxed gallbladder strips, probably via beta 2-adrenoceptor stimulation. Transmural nerve stimulation always caused contractions, but in the presence of atropine inhibitory responses were demonstrable and these were antagonized by propranolol. There was no evidence of non-adrenergic inhibitory neural responses. Of the peptides tested, only cholecystokinin octapeptide (CCK-OP), gastrin, pentagastrin, substance P and caerulein caused contractions. Responses to CCK-OP, gastrin and pentagastrin were antagonized by dibutyryl cyclic GMP. Hormones which had no effect upon human gallbladder strips included motilin, secretin, bombesin, neurotensin, glucagon, vasopressin, VIP and somatostatin. Considerable differences therefore exist between human tissues and those from experimental animals with respect to the direct actions of neural and hormonal stimuli on gallbladder contractility.
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PMID:Contractility of human gallbladder muscle in vitro. 297 88


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