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)

Pancreatic glucagon (PG) and other glucagon-like immunoreactive materials (GLI) were measured in the plasma of normal and of newly diagnosed untreated diabetic children, using an antiglucagon serum (AGS) highly specific for pancreatic glucagon (AGS 18) and an AGS which crossreacts with extracts of intestinal mucosa (AGS 10). Gut GLI was considered to be the difference between "total" GLI (AGS 10) and PG (AGS 18). Glucose and immunoreactive insulin (IRI) were also measured. PG, total GLI and gut GLI were significantly elevated in children with severe insulin insufficiency and were reduced to normal by insulin treatment, even though a significant fasting hyperglycemia was still present. In three diabetic children who had high initial plasma IRI levels the three glucagon fractions were normal. We conclude that insulin insufficiency is characterized not only by high plasma levels of PG as previously reported, but also of gut GLI. These abnormalities can be corrected by the administration of insulin.
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PMID:Glucose, insulin, pancreatic glucagon and glucagon-like immunoreactive materials in the plasma of normal and diabetic children. Effect of the initial insulin treatment. 121 49

The boiling method deviced in accordance with the extraction procedure of secretin was applied to the extraction of gut glucagon-like immunoreactive material (GLI) and compared with the acid alcohol method of Kenny with respect to efficiency of the extraction and property of the extracted materials. GLI was extracted from minced porcine small intestine by each method. The total amount of GLI extracted by the boiling method was 14.45+/-2.07 mug/10g small intestine (mean+/-SE), showing a high yield as compared to 4.07+/-0.29 mug/10 g small intestine obtained by the acid alcohol method. The difference was statistically significant (p less than 0.005). The gel chromatogram of the acid alcohol extract was separated into two peaks; peak 1 appeared before the the insulin marker, while peak II was eluted with the glucagon marker. The chromatogram of the boiling extract has a main broad fraction including insulin marker and a minor second peak corresponding to peak II of the acid alcohol extract. Boiling of the acid alcohol extract did not cause any shift of peak I in chromatogram. GLI present in the first half of the main fraction of the boiling extract was different from that in the latter half, but identical to peak I of the acid alcohol extract with respect to the immunoreactivity against glucagon antibody. It is concluded that in the extraction of GLI not only high yield is achieved but one or more new components is picked up by the boiling procedure as compared to the acid alcohol method.
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PMID:Boiling method for the extraction of gut glucagon-like immunoreactive materials. 123 92

The plasma gastric inhibitory polypeptide (GIP), pancreatic glucagon-like immunoreactivity (PGLI), and gut glucagon-like immunoreactivity (GGLI) responses to oral glucose have been measured in five patients with chronic pancreatitis (with diabetic glucose tolerance tests) and in matched nondiabetic controls. Plasma GIP levels rise rapidly after glucose ingestion before changes in circulating glucose and insulin concentration. Patients with pancreatitis have a greater than normal GIP response to oral glucose, which may account for the relatively unimparied insulin response to oral glucose in these patients compared with that to iv glucose, as has been previously found. Patients with pancreatitis also have a paradoxical rise in PGLI and an exaggerated rise in GGLI concentration following oral glucose.
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PMID:Gastric inhibitory polypeptide (GIP) in chronic pancreatitis. 127 May 74

A brief review is given of the large numbers of hormones in the pancreas and gut. The concept of the 'entero-insular' axis is discussed and a critical appraisal is given of the claims for various proposed insulinotropic gut hormones. Gastric-inhibitory polypeptide appears at the present time to occupy a leading role in the entero-insular axis. Glucagon-like substances and vasoactive intestinal peptide are of importance in glucose homeostasis by having direct effects on carbohydrate metabolism. The study of the release of gut hormones after food ingestion would indicate that pancreatic glucagon exerts control on glucose hemeostasis during food ingestion, whereas gastric-inhibitory polypeptide may regulate insulin secretion after eating.
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PMID:The role of enteric hormones in glucose homeostasis. 127 42

Six non-anaesthetized Large White pigs (mean body weight 59 +/- 1.7 kg) were fitted with permanent catheters in the portal vein, the brachiocephalic artery and the right hepatic vein and with electromagnetic flow probes around the portal vein and the hepatic artery. The animals were provided a basal none-fibre diet (diet A) alone or together with 6% guar gum (diet B) or 15% purified cellulose (diet C). The diets were given for 1 week and according to a replicated 3 x 3 latin-square design. On the last day of each adaptation period test meals of 800 g were given prior to blood sampling. The sampling was continued for 8 h. Guar gum strongly reduced the glucose absorption as well as the insulin, gastric inhibitory polypeptide (GIP) and insulin-like growth factor-1 (IGF-1) production. However, the reduction in peripheral blood insulin levels caused by guar gum was not associated with a change in hepatic insulin extraction. IGF-1 appeared to be strongly produced by the gut. The liver had a net uptake of the peptide. Ingestion of guar gum increased the hepatic extraction coefficient of gut produced IGF-1. Guar gum ingestion also appeared to decrease pancreatic glucagon secretion. Cellulose at the level consumed had very little effect on the parameters considered. It is suggested that the modulation of intestinal mechanisms by guar gum was sufficient to mediate the latter internal metabolic effects.
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PMID:Glucose absorption, hormonal release and hepatic metabolism after guar gum ingestion. 131 55

Six Large White pigs (mean body-weight 59 (SE 1.7) kg) were surgically fitted with permanent catheters in the portal vein, the brachiocephalic artery and the right hepatic vein, as well as with electromagnetic flow probes around the portal vein and the hepatic artery, and allowed to recover. The non-anaesthetized animals were given a basal non-fibre diet (diet A) alone or together with 60 g guar gum/kg (diet B) or 150 g purified cellulose/kg (diet C) by substitution for mica. The diets were given for weekly periods and according to a replicated 3 x 3 Latin square design. On the last day of each such adaptation period, test meals of 800 g were given before blood sampling. Sampling was continued for 8 h. Guar gum strongly reduced glucose apparent absorption without changing the absorption and the hepatic uptake profiles. Production rates of insulin, gastric inhibitory polypeptide and insulin-like growth factor-1 (IGF-1) were lowest after guar gum ingestion. However, the reductions in peripheral blood insulin levels caused by guar gum were not associated with a change in hepatic insulin extraction. IGF-1 appeared to be strongly secreted by the gut, whereas the liver had a net uptake of the peptide. Ingestion of guar gum increased the hepatic extraction coefficient of gut-produced IGF-1. Guar gum ingestion appeared also to decrease glucagon secretion. Cellulose at the level consumed had very few effects on the variables considered. It is suggested that the modulation of intestinal mechanisms by guar gum was sufficient to mediate the metabolic effects described.
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PMID:Effects of guar gum and cellulose on glucose absorption, hormonal release and hepatic metabolism in the pig. 133 69

Patients with liver cirrhosis develop marked abnormalities in small bowel motility and high plasma glucagon levels. Disturbances in small intestinal motor activity could be related to hyperglucagonemia. To investigate the relationship between fasting plasma glucagon levels and changes in small bowel motility in patients with liver cirrhosis, eighteen cirrhotic patients and ten controls were studied. Plasma glucagon was measured by RIA. Mouth to cecum transit time was estimated by lactulose hydrogen breath test. Fasting small bowel motility was investigated by means of intraluminal manometry. Plasma glucagon levels were significantly higher in patients with cirrhosis (61 +/- 5 pmol/l) than in controls (32 +/- 3 pmol/l); p < 0.01. In patients with liver disease, plasma glucagon levels were not significantly correlated to mouth to cecum transit time (r: -0.32), duration of migrating motor complex (r: -0.24), nor to the frequency of multiple clustered contractions (r: -0.26). The degree of small bowel dysmotility is not related to plasma glucagon levels in patients with hepatic cirrhosis. These results do not support the hypothesis that hyperglucagonemia plays an important pathogenic role in the abnormalities of gut motility in cirrhosis.
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PMID:[Are disturbances of small intestinal motility associated with hyperglucagonemia in patients with liver cirrhosis?]. 134 Sep 93

Six types of endocrine cells showing immunolabelling against gut or pancreatic islet hormones were identified in the pancreatic-bile duct system of the normal adult rat at the light and electron microscopic levels. They were located within the epithelial lining of the duct system from the intercalated portion to its duodenal opening. However, the distribution and frequency of each endocrine cell varied along the length of the duct system. While insulin, glucagon, somatostatin, and pancreatic polypeptide cells were widely distributed along the entire duct system, small numbers of cholecystokinin and serotonin cells were confined to the terminal portion. A considerable number of somatostatin cells were concentrated in gland-like pouches of the terminal portion of the common pancreatic-bile duct. When the accessory pancreatic duct was present, insulin, glucagon, and somatostatin cells were also found in its epithelial lining. Electron microscopically, the specific content of the secretory granules of all endocrine cells was confirmed by immunolabelling or cytochemical staining. Further the characteristics of the secretory granules of each endocrine cell type corresponded to those present in the same kind of endocrine cells in gut or pancreatic islet. The duct endocrine cells displayed a particular ultrastructural appearance. The "open type cells" were highly polarized, with their apical cytoplasmic process reaching the duct lumen, whereas "closed type cells" showed long basal cytoplasmic processes with no connection with the duct lumen. In general, insulin, and somatostatin cells were of the "open type", while no morphological connection with the duct lumen was found for glucagon and pancreatic polypeptide cells. The presence of various duct endocrine cells with their particular ultrastructural appearance implies that they may take part in modulating the function of the duct system.
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PMID:Characterization of the endocrine cells in the pancreatic-bile duct system of the rat. 134 74

To clarify changes in gastric acid and gut hormone secretion after pylorus-preserving pancreaticoduodenectomy (PPPD), an experimental study was performed using a model of pylorus-preserving duodenectomy in dogs previously provided with Heidenhain pouch (HP). The duodenectomy involves resection of the duodenum and 10 cm of the proximal jejunum preserving 2 cm of juxtapyloric duodenum and round-shaped duodenal wall around pancreatic papilla. Reconstruction was done by anastomosing the rho-shaped jejunal loop to gallbladder, juxtapyloric duodenum and peripapillar round-shaped duodenal wall with ligation of the common bile duct. For these dogs, intravenous glucose tolerance test (IVGTT), oral glucose tolerance test (OGTT), meal ingestion test (TM) and histological studies of pancreatic specimen obtained at autopsy were performed investigating pancreatic, gastric acid and gut hormone secretion. Preservation of endocrine and exocrine pancreatic secretion after operation demonstrated our experimental model to be adequate for evaluation of the factor of duodenectomy in PPPD on gastric acid and gut hormone secretion avoiding the influences of changes in pancreatic secretion. Postprandial gastric acid secretion from HP did not change significantly after operation. Postprandial secretion of gastrin, glucagon, GIP and enteroglucagon did not alter significantly after operation. These results indicated that in the clinical PPPD procedure, preservation of more than 2 cm of duodenum from the pylorus produced neither postprandial gastric acid hypersecretion, which might be cause of postoperative stomal ulcer, nor any change of related gut hormone secretion.
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PMID:An experimental study on the gastric acid and gut hormone secretion after pylorus preserving duodenectomy in dogs. 135 8

Glucagon-like peptide 1 (GLP-1)(7-36) amide, a member of the family of glucagon and related peptides, synthesized by intestinal L cells, has a well-defined distribution in rat brain. In addition, specific GLP-1(7-36) amide receptors have also been localized in some regions of the brain, which suggests that this novel gut-brain peptide has a role in brain function. Accordingly, we investigated the effects of this peptide on the release of amino acid neurotransmitters in the basal ganglia of conscious rats after its perfusion through a concentric "push-pull" cannula system with an artificial cerebrospinal fluid. To obtain stable basal levels of amino acids, the basal ganglia were perfused with an artificial cerebrospinal fluid for 2 h at a flow rate of 20 microliters/min and then with GLP-1(7-36) amide for 10 min, followed by 40 min poststimulation perfusion. GLP-1(7-36) amide produced an immediate increase (p less than 0.01) of the extracellular levels of glutamine and glutamic acid in the basal ganglia. By contrast, this peptide has no effect on the levels of aspartic acid, glycine, and serine. Because glutamine is a metabolic precursor of glutamic acid and is synthesized almost exclusively in astrocytes, these findings suggest a stimulatory effect of GLP-1(7-36) amide on astrocytes and/or neurons of the rat basal ganglia.
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PMID:Selective release of glutamine and glutamic acid produced by perfusion of GLP-1 (7-36) amide in the basal ganglia of the conscious rat. 135 98


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