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 present study was designed to determine in humans the dose of CCK which suppresses food intake. 18 male subjects received in randomized order either i.v. saline or Thr28 Nle31 CCK 25-33 (CCK-9) at 100 or 500 pmol/kgh, respectively. In addition, 7 subjects received CCK together with the opiate receptor antagonist naloxone to examine if activation of endogenous opioids might interfere with the potential satiating effect of CCK. Food intake during saline was 32 +/- 2 sandwiches (mean +/- SEM), during CCK-9 100 pmol/kgh 28 +/- 2 (n.s.) and only 12 +/- 3 during CCK-9 500 pmol/kgh (p less than 0.01). The respective water intake was 730 +/- 70 ml, 590 +/- 60 ml (n.s.) and 320 +/- 50 ml (p less than 0.01). Naloxone further reduced food and water intake during high but not low dose CCK or saline. During saline postprandial insulin levels rose by 49 +/- 6 microU/ml within 45 min which was attenuated during low dose (23 +/- 6 microU/ml; p less than 0.01) and high dose CCK-9 (1 +/- 1 microU/ml; p less than 0.001). Plasma glucagon did not change in control or CCK experiments. The postprandial rise of pancreatic polypeptide was attenuated during high dose CCK. Naloxone had no effect on the hormonal response except for a prolonged reduction of insulin and glucose levels following high dose CCK + naloxone. Plasma CCK levels rose by 5.4 pmol/l in controls but by 55 and 255 pmol/l during the low and high dose CCK infusion, respectively. These data demonstrate that suppression of food intake in man by i.v. CCK is a pharmacological rather than a physiological effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of CCK on food intake in man: physiological or pharmacological effect? 171 70

HPLC-purified 125I-labeled vasoactive intestinal peptide (VIP) bound in a specific, saturable, and reversible manner to pancreatic plasma membranes isolated from newborn calves, from milk-fed calves at 28 and 119 days, and from weaned calves at 119 days. A series of VIP analogues, including pituitary adenylate cyclase-activating polypeptide (PACAP), displaced 125I-VIP binding and activated adenylate cyclase in the same order of relative potency: PACAP-38 greater than helodermin greater than VIP, PACAP-27 greater than PHM (human peptide with NH2-terminal histidine and COOH-terminal methionine amide). At maximally effective concentrations, these five peptides produced the same two- to threefold increase of adenylate cyclase activity in pancreatic membranes from newborn and 28-day-old calves, and fourfold in ruminant or preruminant animals at 119 days. The activation constant for PACAP-38 ranged from 0.1 to 0.34 nM throughout the postnatal development. Helospectin I and II were three times less potent than VIP in inhibiting 125I-VIP binding. At concentrations up to 0.1 microM, secretin, rat and human growth hormone-releasing factors, glucagon, oxyntomodulin, the truncated form of glucagon-like peptide-1 lacking the 6 NH2-terminal amino acid sequence (TGLP-1), GLP-2, gastric inhibitory peptide, gastrin, CCK, and insulin had no effect on binding. Scatchard plots from 28- and 119-day-old calves were compatible with the presence of two classes of 125I-VIP binding sites: one with a high affinity for VIP and a low binding capacity (Kd = 0.11-0.4 nM, Bmax = 66-174 fmol/mg protein) and the other with a low affinity and high binding capacity. At birth, only one class of binding sites was observed (Kd = 0.4 nM, Bmax = 858 fmol/mg protein). The covalently cross-linked PACAP-preferring 125I-VIP binding site is a glycoprotein of 55 kDa with higher sensitivity to PACAP vs. helodermin and VIP. Our results suggest that calf pancreatic functions might be regulated at an early stage of postnatal development by PACAP receptors linked to cAMP generation.
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PMID:Characterization of binding sites for VIP-related peptides and activation of adenylate cyclase in developing pancreas. 184 91

The effects of porcine pancreastatin on insulin release stimulated by insulinotropic agents, glucagon, cholecystokinin-octapeptide (CCK-8), gastric inhibitory polypeptide (GIP) and L-arginine, were compared to those of bovine chromogranin A (CGA) using the isolated perfused rat pancreas. Pancreastatin significantly potentiated glucagon-stimulated insulin release (first phase: 12.5 +/- 0.9 ng/8 min; second phase: 34.5 +/- 1.6 ng/25 min in controls; 16.5 +/- 1.1 ng/8 min and 44.0 +/- 2.2 ng/25 min in pancreastatin group), whereas CGA was ineffective. The first phase of L-arginine-stimulated insulin release was also potentiated by pancreastatin (6.9 +/- 0.5 ng/5 min in controls, 8.4 +/- 0.6 ng/5 min in pancreastatin group), but not by CGA. Pancreastatin did not affect CCK-8 or GIP-stimulated insulin release. Similarly, CGA did not affect insulin release stimulated by CCK-8 or GIP. These findings suggest that pancreastatin stimulates insulin release in the presence of glucagon. Because pancreastatin can have multiple effects on insulin release, which are dependent upon the local concentration of insulin effectors, pancreastatin may participate in the fine tuning of insulin release from B cells.
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PMID:Effects of pancreastatin and chromogranin A on insulin release stimulated by various insulinotropic agents. 185 78

We studied the cellular distribution of glucagon-like peptide-1 (GLP-1) in the pancreas and gut and the effects of GLP-1 and its truncated form, GLP-1(7-36) amide, on basal and stimulated insulin and glucagon secretion in the mouse. Immunofluorescence staining showed that GLP-1 immunoreactivity occurred within peripheral islet cells and in cells located mainly distally in the small intestine and in the entire large intestine. Double-immunostaining revealed that the GLP-1-immunoreactive cells were identical to the glucagon/glicentin cells. Experiments in vivo revealed that basal insulin secretion was stimulated by GLP-1(7-36) amide at the dose levels of 8 and 32 nmol/kg, and by GLP-1 at 32 nmol/kg. Furthermore, GLP-1(7-36) amide showed additive stimulatory influence with glucose (2.8 mmol/kg), the cholinergic agonist carbachol (0.16 mumol/kg), and the C-terminal octapeptide of cholecystokinin (CCK-8, 5.3 nmol/kg), when injected at 8 or 32 nmol/kg. In contrast, stimulated insulin secretion was unaffected by GLP-1. Moreover, the glucagon secretory responses to carbachol and CCK-8 were inhibited by GLP-1(7-36) amide but were unaffected by the entire GLP-1. We conclude that GLP-1(7-36) has the potential for being a modulator of islet hormone secretion.
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PMID:GLP-1 and GLP-1(7-36) amide: influences on basal and stimulated insulin and glucagon secretion in the mouse. 188 89

The present study was undertaken to evaluate the changes of gastrointestinal hormones and pancreatic functions after major pancreatectomy in dogs and human. After more than 92% pancreatectomy in dogs, all dogs developed diabetes mellitus (DM). In these dogs, the remnant pancreas showed poor regeneration rate of 24.0% at 6 weeks, decreased sigma IRI in IV-GTT had not been recovered, pancreatic glucagon response was diminished, pancreatic exocrine function had been declined with increased plasma levels of secretin and CCK, and gastric secretion increased in spite of diminished gastrin response. After 74 to 92% pancreatectomy, 17.6% of dogs developed DM. The dogs with DM had poor pancreatic regeneration rate of 22.7% at 12 weeks, hypersecretion of glucagon and decreased gastric secretion with low plasma concentration of gastrin. On the other hand, in dogs without DM, pancreatic regeneration rate showed 42.7% at 12 weeks, insulin release and pancreatic exocrine function had been recovered well, and plasma CCK levels increased without changes of gastric secretion. In the clinical study, gastric secretion, CCK response and pancreatic endocrine and exocrine functions had been maintained better after pylorus preserving pancreaticoduodenectomy than after conventional pancreaticoduodenectomy.
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PMID:[Clinical and experimental studies on pancreatic functions and gastrointestinal hormones after major pancreatectomy]. 194 87

Cholecystokinin is a choleretic in dogs. Some of the effects of cholecystokinin in stimulating bile flow in dogs are produced by cholecystokinin stimulating the release of other choleretic hormones such as insulin and glucagon. The purpose of this study was to determine the effects of cholecystokinin receptor antagonists on canine hepatic bile flow and insulin and glucagon release from the pancreas. Cholecystokinin octapeptide (CCK-8) and intraduodenal fat were administered to dogs that had undergone cholecystectomy with chronic biliary fistulas with and without the administration of cholecystokinin receptor antagonists. Bile secretion and systemic venous insulin, glucagon, and cholecystokinin levels were measured. The cholecystokinin receptor antagonists benzotript and CR 1409 had no effect on bile flow or hormone levels when administered without cholecystokinin, whereas proglumide produced a large increase in bile flow without altering hormone levels. The response produced by proglumide may be the result of an osmotic effect produced by the substance being secreted in bile and its stimulating bile salt secretion in bile. CCK-8 and intraduodenal fat increased bile flow, bile chloride secretion, and cholecystokinin, insulin, and glucagon concentrations in venous blood. The cholecystokinin receptor antagonists benzotript and CR 1409 significantly decreased the bile flow and insulin and glucagon changes produced by exogenous CCK-8. The effect of intraduodenal fat on bile flow was not inhibited by the cholecystokinin receptor antagonists, whereas the increased insulin and glucagon levels were decreased significantly. Intraduodenal fat may release other choleretic hormones not affected by cholecystokinin receptor antagonists. The choleresis produced by exogenous CCK-8 is inhibited by cholecystokinin receptor antagonists, perhaps by inhibiting the release of the choleretic hormones insulin and glucagon.
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PMID:The effect of cholecystokinin-receptor antagonists on cholecystokinin-stimulated bile flow in dogs. 200 May 61

Feeding responses to continuous intravenous administration of graded doses of the COOH-terminal octapeptide of cholecystokinin (CCK-8) and pancreatic glucagon, alone and in combination, were determined in dogs fasted 4 h. Low doses of glucagon (50, 500, 5,000, 6,000 pmol.kg-1.h-1) had no effect on food intake, whereas higher doses (12 and 24 nmol.kg-1.h-1) depressed intake by 50-60%. Of the CCK-8 doses administered (50 and 400 pmol.kg-1.h-1), food intake was depressed only at the higher dose (53%). This effect was blocked by glucagon (50-5,000 pmol.kg-1.h-1). Simultaneous administration of 50 or 500 pmol.kg-1.h-1 of glucagon and 50 pmol.kg-1.h-1 of CCK-8, doses currently thought to produce plasma peptide levels similar to those occurring postprandially in dogs, had no effect on food intake. These results suggest that plasma levels of CCK and glucagon after a meal are not sufficient alone or in combination to produce satiety.
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PMID:Interaction of cholecystokinin-8 and pancreatic glucagon in control of food intake in dogs. 201 41

In the present study we demonstrate by immunohistochemical techniques that calcitonin gene-related peptide (CGRP) is present in nerve terminals in the islets of Langerhans. Furthermore, binding studies with 125I-CGRP indicate that dispersed acini from guinea pig pancreas contain a single class of high-affinity binding sites for CGRP with an apparent dissociation constant of 18 nM. Vasoactive intestinal peptide (VIP), rat growth hormone-releasing factor (rGRF), cholecystokinin octapeptide (CCK-OP), and bombesin do not interact with these receptors. Interaction of CGRP with these receptors leads to release of amylase from the acinar cells. Amylase release is half maximal at 0.3 nM CGRP and maximal at 3 nM CGRP. Maximal amylase release with CGRP is one-third of that observed with VIP. CGRP-induced amylase release is dependent on theophylline in the incubation medium. CGRP potentiates the amylase release stimulated by bombesin and CCK-OP but has no effect on amylase release stimulated by VIP, rGRF, and natural glucagon. CGRP stimulates a 25% increase in basal cellular cAMP. These results indicate that guinea pig pancreatic acinar cells contain a novel receptor for CGRP and that interaction of CGRP with this receptor leads to digestive enzyme secretion through a cAMP-mediated pathway. The presence of CGRP in the islets of Langerhans suggests a pathway for CGRP to reach the exocrine pancreas through an insuloacinar portal system.
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PMID:Receptor for calcitonin gene-related peptide: binding to exocrine pancreas mediates biological actions. 240 16

Twenty medullary carcinomas of the thyroid gland were examined for the presence of immunoreactive calcitonin, thyroglobulin, glucagon, keratin, gastrin/CCK, carcinoembryonic antibody (CEA), insulin, serotonin, adreno-corticotropic hormone (ACTH), prostatic acid phosphatase, and somatostatin using the immunoperoxidase peroxidase-antiperoxidase technique. In addition, they were stained with mucicarmine, alcian blue/periodic acid-Schiff (PAS), Grimelius, Congo red, crystal violet, and Fontana-Masson stains. Calcitonin-immunoreactive cells were absent in one tumor and present in 19 tumors (95%). Thyroglobulin was present in seven tumors (35%). Twenty tumors contained CEA-immunoreactive cells (100%). Fourteen cases were immunoreactive to serotonin (70%) and 12 were positive for somatostatin (60%). Glucagon- and gastrin/CCK-immunoreactive cells were found in two cases each (10%). Four tumors (20%) contained ACTH-immunoreactive cells and three cases (15%) were positive for prostatic acid phosphatase. Five cases (25%) contained keratin-immunoreactive cells. One case was immunoreactive to insulin (5%). Grimelius-positive cells were present in 19 of the cases (95%). Mucin-containing cells were present in 65% of the cases. The validity of the immunocytochemical localizations was tested by specific absorption of each antibody with the corresponding antigen. The demonstration of immunoreactivity for multiple antigens in each of the 20 cases suggests that the origin of medullary thyroid carcinomas is from a neuroendocrine cell potentially capable of producing numerous hormone substances. In addition, as the neoplastic cells in 35% of the tumors contained hormonal substances as well as thyroglobulin, it is suggested that papillary or follicular tumors mixed with a neuroendocrine component exist more commonly than previously suspected. Finally, psammoma bodies might be present in pure medullary carcinoma of the thyroid gland.
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PMID:Medullary carcinoma of the thyroid gland. Clinical, pathological, and immunohistochemical features with review of the literature. 241 97

The cochleae of juvenile guinea pigs were investigated for the presence of several neuropeptides. Glucagon, insulin, CCK and beta-endorphin immunoreactive neurons and nerve fibers as well as hair cells were demonstrated by the peroxidase antiperoxidase technique. Small amounts of substance P were also found in different sites in the inner ear. In contrast, prolactin-like material could not be found at all. These findings have significance with regard to the putative role of neuropeptides in neuromodulation.
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PMID:Immunocytochemical detection of peptides in the guinea pig cochlea. 242 64


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