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)

A 28-year-old man presented with epigastric pain and obstructive jaundice associated with a histologically and immunologically unusual variant of carcinoid tumor involving the ampulla of Vater. The tumor contained abundant psammoma bodies and exhibited immunoreactivity only for somatostatin. Immunoperoxidase studies for insulin, glucagon, vasoactive intestinal peptide, calcitonin, serotonin, and ACTH had negative results. In contrast to most somatostatinomas of pancreatic origin, clinically this ampullary somatostatinoma was not accompanied by features of the somatostatinoma syndrome. A literature review of the clinical and hormonal features in reported cases of gastrointestinal and pancreatic somatostatinomas is presented.
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PMID:Ampullary somatostatinoma: psammomatous variant of gastrointestinal carcinoid tumor--an immunohistochemical and ultrastructural study. Report of a case and review of the literature. 631 1

Eleven patients after total pancreatectomy and 68 patients after pancreatoduodenectomy were reviewed for evaluating the importance of nutritional management after massive resection of the pancreas. Nutritional supply by IVH resulted in maintaining and improving the hepatic function under obstructive jaundice in clinical and experimental studies. Administration of elemental diet after the operation shortened the period of IVH, and had a effect to spare the requirement of exogenous insulin. One of the most important problems after pancreatectomy with extensive dissection of the lymph nodes and the nerves around superior mesenteric artery was a malnutrition which appeared frequently after long term follow-up. The malnutrition should be treated by IVH as soon as possible for preventing further aggravation of digestive and absorptive function of the alimentary tract. Oral or nasogastric tube administration of elemental diet is useful for weaning the patient from IVH, and it serves to prevent subsequent development of malnutrition. In six totally pancreatectomized patients studied, postabsorptive plasma concentration of Arg., Lys., Thr., Ala., Gly., Ser. and Pro. were greatly elevated compared to normal value, however these abnormalities were normalized by 1 to 3 mg of glucagon administration. Glucagon administration resulted in no significant change in daily nitrogen balance.
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PMID:[Nutritional management after massive resection of the pancreas]. 643 88

Glucagon has a choleretic effect and also stimulates energy-consuming reactions, such as gluconeogenesis and ureogenesis in the liver. The effect of glucagon on energy metabolism in the liver was analyzed in rabbits with obstructive jaundice that had severe liver damage, indicated by significantly lower hepatic energy charge levels. The gluconeogenetic responses to glucagon administration, as shown by increases in the plasma glucose levels, were usually observed in normal rabbits, but these responses were completely depressed after glucagon administration in rabbits with obstructive jaundice. The energy charge levels in the latter animals decreased even further after glucagon administration. Even though the energy consumption for gluconeogenesis after glucagon administration was limited in the jaundiced rabbits, it was sufficient to cause a deterioration in the hepatic energy balance. The above findings show that the administration of glucagon increases the amount of energy expended in the liver following a reduction in the hepatic energy charge in rabbits with obstructive jaundice. Therefore, even though glucagon has a choleretic effect, it should be administered carefully to patients with obstructive jaundice, especially in those with severe liver damage, such as in patients with cholangitis.
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PMID:Glucagon responses in rabbits with obstructive jaundice and a low energy status in the liver. 777 10

To examine the mechanism of reduced tolerance to glucose in obstructive jaundice, insulin and glucagon metabolism was examined using mongrel dogs. Perfused pancreas isolated from obstructive jaundice dogs was used for this purpose, and the following results were obtained. Insulin release from the pancreas was decreased but glucagon was not changed by stimulation with cholecystokinin octapeptide. Extraction of insulin and glucagon in the liver was examined using the dogs which had cholestatic and non-cholestatic lobes in each individual. Insulin levels of the hepatic blood were significantly lower than those of the portal blood. In comparison of the insulin levels between the hepatic blood from cholestatic and non-cholestatic lobes, the value of the cholestatic hepatic blood was significantly higher than that of the non-cholestatic hepatic blood. Concerning on glucagon, however, there were no significant differences between the two blood samples. Therefore, the reduced tolerance to glucose in obstructive jaundice could not be attributed to the enhanced extraction of insulin in the liver but to the decrease of insulin production in the pancreas.
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PMID:[Experimental study on the metabolism of pancreatic hormone in obstructive jaundice]. 812 91

Insulin and glucagon metabolism in the pancreas with obstructive jaundice caused by complete ligation of the common bile duct and in the cholestatic liver caused by hepatic duct ligation was evaluated experimentally using dogs. The isolated perfused pancreas in obstructive jaundiced dogs, which showed a low insulin response in the peripheral blood after intravenous glucose administration, revealed depression of insulin production and no change of glucagon production in response to cholecystokinin octapeptide. The extraction of insulin in the cholestatic lobe of the liver was decreased compared with that in the noncholestatic lobe. The extraction of glucagon, on the other hand, in the cholestatic lobe and in the noncholestatic lobe showed no significant difference. So the imbalance of glucose metabolism in obstructive jaundice does not depend on the enhanced extraction of insulin in the liver, but on the depression of insulin production in the pancreas.
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PMID:Metabolism of insulin and glucagon in liver and pancreas in dogs with obstructive jaundice. 846 Jan 1

We performed 75 laparoscopic cholecystectomies during July and September 1996. In 3 men and 4 women, aged 32-87 years, there was obstructive jaundice caused by choledocholithiasis. During laparoscopy in the jaundiced patients, calculi were identified by cholangioscopy and intra-operative cholangiography. They were washed into the duodenum (confirmed cholangiographically) after intravenous glucagon injections and dilation of the papilla of Vater. Serum bilirubin and liver enzyme levels returned to normal within a few days. There was no operative or postoperative morbidity, nor any biliary-related systemic complications. Average postoperative hospitalization was 3 days.
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PMID:[Laparoscopy for common bile duct stones]. 1095 66

Hyperglycemia associated with obstructive jaundice seriously affects the prognosis of patients with hepatobiliary diseases. We investigated secretory properties of isolated islets from bile duct-ligated (BDL) rats. Pancreatic islets from BDL rats lost their secretory responses to glucagon-like peptide-1 (GLP-1), although their responses to glucose were normal. Loss of potentiation of insulin release was also observed in glucagon and glucose-dependent insulinotropic peptide (GIP), whereas modulation of the release by forskolin, dibutyryl cAMP, or epinephrine remained unaffected. cAMP production by BDL islets was not increased by these insulinotropic hormones. Serum levels of glucagon, but not GIP, were increased in BDL rats. GLP-1 levels were also elevated, although they did not reach statistical significance. Immunoblotting of trimeric G protein subunits demonstrated that G(s)alpha L and G(s)alpha S, but not G(i)alpha 1/2 and G(i)alpha 3/o alpha, were less expressed in BDL islets. Therefore, unresponsiveness of the beta-cell to cAMP-raising hormones is involved in glucose intolerance under cholestasis. It results from diminished expression of alpha-subunits of the relevant G protein, G(s), and desensitization of receptors of these hormones.
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PMID:Lack of effect of incretin hormones on insulin release from pancreatic islets in the bile duct-ligated rats. 1112 Jun 59


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