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)

Human insulin and glucagon mRNA were identified in routinely processed pancreatic tissue by non-radioactive in-situ hybridization using digoxigenin-labelled oligonucleotide probes. Cocktails of synthetic oligonucleotides complementary to human insulin and glucagon mRNA were labelled with digoxigenin using terminal deoxynucleotidyl transferase (Tdt). Specific hybrids were detected with alkaline phosphatase-labelled anti-digoxigenin antibody and visualized by BCIP-nitroblue tetrazolium indicator substrate. The results showed highly sensitive and specific staining of islet cells on a range of routinely formalin-fixed and paraffin-embedded tissues. Post-mortem pancreatic tissue from adults and stillborn neonates yielded acceptable signals as long as tissue morphology was well preserved. Preliminary investigations using pancreatic endocrine cell tumours gave clear easily interpretable signals which were comparable to conventional immunostaining. The application of this technique promises to be of value in the investigation of pancreatic disease.
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PMID:Demonstration of insulin and glucagon mRNA in routinely fixed and processed pancreatic tissue by in-situ hybridization. 168 4

The possible trophic influence of the capsaicin-sensitive extrinsic innervation of the gastrointestinal mucosa was investigated. Rats were treated neonatally with capsaicin. The gastrointestinal content of serotonin and glucagon-like immunoreactivity were used as a measure of the effect on the endocrine gut mucosa and gastrointestinal aminopeptidase and alkaline phosphatase activities were used as a measure of the effect on the gut brush-border. The gastrointestinal content of the neuropeptides substance P, VIP and CGRP were used to monitor effects on the innervation of the gut. The depletion of substance P-immunoreactivity(-IR) and calcitonin gene-related peptide(CGRP)-IR in extracts of urinary bladder and lung from the capsaicin-treated rats is evidence of the efficacy of capsaicin treatment in affecting a loss of C-fibre sensory nerves. The significant depletion of CGRP-IR measured in the stomach and duodenum of capsaicin-treated rats indicated the loss of the C-fibre sensory innervation to the gastrointestinal tract. The gastrointestinal content of VIP and substance P, which are predominantly within intrinsic gut neurones, were unaffected by capsaicin treatment. In all regions of the gastrointestinal tract of capsaicin-treated rats, the serotonin and glucagon-IR levels were not significantly different from those in controls. Similarly the levels of activity of the brush-border enzymes were not significantly effected by capsaicin treatment. This suggest the absence of any major trophic influence of capsaicin-sensitive sensory nerves on the gut endocrine mucosa and the brush border.
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PMID:Regulatory peptide and serotonin content and brush-border enzyme activity in the rat gastrointestinal tract following neonatal treatment with capsaicin; lack of effect on epithelial markers. 170 47

Eighteen healthy dogs were allotted to 3 groups (n = 6 dogs each). All dogs were evaluated at the beginning of the study by complete physical examination; total and differential WBC counts; serum biochemical analysis (alanine transaminase and alkaline phosphatase activities and bilirubin and albumin concentrations); sulfobromophthalein excretion, ammonia tolerance, and glucagon response testing; portal and intraparenchymal pressure determinations; operative mesenteric portography; and histologic assessment of hepatic biopsy specimens. The left hepatic vein was ligated completely in dogs of groups 1 and 2. Group-3 (control) dogs had a ligature placed loosely around the left hepatic vein. Dogs of groups 1 and 3 were reevaluated 24 hours after surgery by use of the aforementioned hematologic and biochemical tests. Group-1 dogs were reevaluated by use of portal and intraparenchymal pressure determinations, jejunal vein portography, and complete necropsy at 48 hours after surgery. At 4 weeks after surgery, dogs of groups 2 and 3 were reevaluated by use of all aforementioned tests. Results indicated transient hepatic congestion, which resolved by the fourth postoperative week. Longstanding effect on hepatic structure, circulation, or function was not found. We concluded that left hepatic vein ligation in clinically normal dogs does not cause severe or permanent liver damage.
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PMID:Effect of left hepatic vein ligation on hepatic circulation, function, and microanatomy in dogs. 185 5

A newly recognized disease in dogs, ulcerative dermatosis associated with diabetes mellitus (diabetic dermatopathy), was diagnosed in 2 dogs with pancreatic endocrine tumors that had immunohistologic evidence of glucagon production. Dogs developed diabetes mellitus in the later stages of the illness, months after the skin disease was first observed. Liver disease was identified and characterized by high serum alkaline phosphatase and alanine transaminase activities. Clinically, erythema and crusting involved the footpads, the face, perioral and genital skin, and ventrum. Histologically, skin lesions were intercellular and intracellular edema and necrosis of the upper half of the epidermis and diffuse parakeratosis. Clinically and histologically, skin lesions closely resembled necrolytic migratory erythema of people, a skin disease that usually is associated with a glucagon-secreting pancreatic endocrine tumor and diabetes mellitus (glucagonoma syndrome): The morphologically descriptive term, superficial necrolytic dermatitis, was preferred over the previously proposed names hepatocutaneous syndrome and diabetic dermatopathy, which each connote only a single feature of the disease.
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PMID:Glucagon-producing pancreatic endocrine tumors in two dogs with superficial necrolytic dermatitis. 227 59

Fractions of isolated epithelial cells were harvested from a segment of porcine jejunum by ten successive incubations with a chelating buffer. The cell fractions showed a progressive decrease in the activity of the brush-border enzymes, alkaline phosphatase and sucrase, with increasing incubation number but a progressive increase in the ability to incorporate labelled thymidine into DNA. Fractions enriched in cells from the crypt region (fractions 9 and 10) contained higher concentrations per mg protein of somatostatin-like immunoreactivity (1.8-fold), glucagon-like immunoreactivity (5.3-fold) and serotonin (3.0-fold) than fractions enriched in cells from the villus tip (fractions 1 and 2). Analysis of extracts of the fractions by gel filtration/radioimmunoassay showed that somatostatin-28 represented the predominant molecular form of somatostatin-like immunoreactivity in all cell fractions but the relative proportion of somatostatin-14 (and related metabolites) to somatostatin-28 was significantly higher (P less than 0.05) in fractions enriched in villus cells (fraction 1 and 2) than in fractions enriched in crypt cells (fractions 5-10). This result suggests that metabolism of somatostatin-28 to somatostatin-14 takes place during migration of the D cell from the crypt base to the villus tip. Heterogeneity in the somatostatin-14 region of the chromatograms indicates that the peptide may be further metabolized by the action of aminopeptidases.
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PMID:Conversion of somatostatin-28 to somatostatin-14 during maturation of epithelial cells in the porcine jejunum. 286 59

The regulation of different maturational processes in the liver is believed to be influenced by the hormonal system. The aim of this study was to investigate the effect of two hormones, glucagon and dexamethasone, on levels of plasma membrane proteins in rat liver cells during late fetal and early postnatal stages of development. For this purpose, 18-day-old rat fetuses and 1-day-old newborns were treated with glucagon or dexamethasone and killed at 22 days of gestation and 3, 5 and 7 days of age, respectively. Postnuclei liver membranes were isolated using a sucrose gradient method and assessed for levels of specific membrane proteins. Asialoglycoprotein receptor and 110,000 Mr glycoprotein, denoted GP 110, representing the sinusoidal and bile canalicular domains, respectively, were quantitated using the immunoblot method. Membrane enzymes alkaline phosphatase, leucine aminopeptidase and gamma-glutamyl transferase were evaluated using enzymatic methods. The data showed that glucagon and dexamethasone have a differential effect on membrane constituents according to the stage of development. Glucagon increased the levels of membrane enzymes during the late fetal stage but had no effect on liver membrane proteins in the newborn animal. In contrast, although dexamethasone elevated GP 110 in fetal rat livers, none of the other marker proteins was significantly affected. On the other hand, in newborns dexamethasone reduced the amount of asialoglycoprotein receptor and alkaline phosphatase and leucine aminopeptidase enzyme activities but greatly augmented the level of gamma-glutamyl transferase. Thus, glucagon primarily affects plasma membrane proteins in late gestation while dexamethasone does so during the early postnatal period. The roles that these two hormones may play during ontogeny is discussed with respect to liver development.
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PMID:The effect of dexamethasone and glucagon on the expression of hepatocyte plasma membrane proteins during development. 289 49

The cytochemical localization of alkaline phosphatase (ALPase) activity and the autoradiographic distribution of glucagon receptors were examined in the plasma membrane of cultured mouse hepatocytes. After 24 hours of culture, ALPase activity was exclusively localized on the plasma membrane in areas of cell-cell contact, and glucagon receptors were more numerous in the plasma membrane at the periphery of re-formed cell trabeculae. These results indicate that plasma membrane regionalization of hepatocytes, lost by cell isolation, reappeared during culture. The cells maintained this plasma membrane regionalization until 48 hours of culture. By 72 hours of culture, however, ALPase activity was seen on the external surface of all regions of plasma membrane, and the glucagon receptors decreased markedly in number and became scattered in all regions of plasma membrane. Thus, the re-formed plasma membrane regionalization disappeared in the cells by 72 hours of culture.
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PMID:Plasma membrane reregionalization in cultured mouse hepatocytes. 300 46

We describe an abrupt increase (at 32 degrees ) in the energy of activation for the reaction of hepatic adenylyl cyclase in the presence of glucagon or epinephrine. This increase is not seen in the presence of fluoride, prostaglandin E(1), or 1-propanol, or in the absence of cyclase stimulators. The change in energy of activation found with hormones is abolished by 1-propanol. This change does not represent differences in hormone or substrate binding at different temperatures, but seems to reflect interactions among elements of the cyclase stimulation sequence. Similar changes in energy of activation were not observed for alkaline phosphatase, cyclic AMP-phosphodiesterase, 5'-nucleotidase, or ouabain-sensitive ATPase. Since the mole fraction of cholesterol in liver membranes is sufficiently high to preclude a phase change in bulk membrane lipids, our observation suggests either that cyclase is restricted to cholesterol-poor membrane regions or that the change in its energy of activation is largely restricted to protein components of the cyclase apparatus. The data are compatible with fundamental differences in the stimulation process(es) for the hormones (glucagon and epinephrine) as compared with those for fluoride and prostaglandin E(1).
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PMID:A temperature-sensitive change in the energy of activation of hormone-stimulated hepatic adenylyl cyclase. 435 55

The present studies were undertaken to determine the role, if any, of cyclic 3',5'-adenosine monophosphate (cyclic AMP) as a chemical inducer of rat liver alkaline phosphatase. Cholera enterotoxin, given intravenously to rats, led to a rapid rise in the activity of hepatic adenyl cyclase that was 7(1/2) times greater than control values in 6 h. Cyclic AMP levels were also significantly increased above control values while the activity of cyclic nucleotide phosphodiesterase was unchanged. Hepatic alkaline phosphatase activity was increased 5(1/2) times above control in 12 h, but its rise followed that of adenyl cyclase and cyclic AMP by several hours. Cycloheximide inhibited the rise of hepatic alkaline phosphatase but not that of adenyl cyclase. The administration of glucagon, a known stimulator of hepatic adenyl cyclase, and of dibutyryl cyclic AMP, led to similar striking increases in hepatic alkaline phosphatase activity. This alkaline phosphatase increase was blocked by the prior administration of cycloheximide. Bile duct ligation, a known stimulator of hepatic alkaline phosphatase activity, failed to produce any significant changes in adenyl cyclase or cyclic AMP. Concomitant treatment of rats with bile duct ligation and cholera enterotoxin or bile duct ligation and glucagon, had no additive effect on the increase in hepatic alkaline phosphatase activity, although the increase occurred earlier. These results suggest that: (a) cyclic AMP may act as an inducer of hepatic alkaline phosphatase: (b) the stimulation of hepatic alkaline phosphatase by cholera enterotoxin is mediated by cyclic AMP; (c) the rise in hepatic alkaline phosphatase following bile duct ligation is not mediated by cyclic AMP; (d) the same alkaline phosphatase in rat liver may be induced by two (or more) mechanisms, only one of which requires cyclic AMP.
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PMID:Alkaline phosphatase. Possible induction by cyclic AMP after cholera enterotoxin administration. 435 3

Glucagon given by intravenous infusion at a dosage of 0.2 to 0.8 mg/hour to four patients with Paget's disease of bone resulted in a dramatic fall in plasma alkaline phosphatase. This was associated with a fall in 24-hour urinary calcium and in total urinary hydroxyproline excretion and a marked relief of bone pain.GLUCAGON MAY INDUCE THESE CHANGES BY THREE POSSIBLE MECHANISMS: (1) by stimulating release of calcitonin; (2) by a direct action of the hormone on bone; and (3) by stimulation of certain bone pyrophosphatases, thus altering the local mechanisms controlling the rate of bone formation and resorption.
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PMID:Glucagon in the treatment of Paget's disease of bone. 512 17


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