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 pancreas of the fetal rat was collected from the first appearance of the pancreatic bud at 11 days of gestation, and every day thereafter until birth. After birth the neonatal pancreas was collected every day for one week, and at intervals thereafter. Fetal B-cells were stained with Gomori's aldehyde fuchsin at 16 1/2 days, and with the immunofluorescent technique for insulin at 14 days. The A-cells were stained as early as 13 days using the fluorescent antibody technique for glucagon. The D-cells first stained at 17 days with pseudoisocyanin. A 4th cell type was found which stained black with silver nitrate, using a method derived from the Grimelius technique for A-cells. This 4th cell type appeared at 15 days in the fetus, reaching its greatest abundance around 19 days, and then declined in numbers after birth until adulthood, when occasionally one or two cells were found.
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PMID:Ontogeny of four cell types in fetal rat islets using histochemical techniques. 78 27

A pancreatic polypeptide with some hormonal properties has been purified from chicken and turkey pancreas using acid-ethanol extraction, gel filtration and anion-exchange chromatography. The material has been crystallised. The crystals are monoclinic with space group C2. Preliminary isomorphous replacement experiments have so far provided a single-site derivative with Hg(NO3)2. A low-resolution electron density map phased with this derivative using anomalous scattering considered together with Patterson function calculations suggest that the molecules are partly helical and are arranged as a compact dimer about the crystallographic two-fold axis. The structure and association of these molecules are compared with those of insulin and glucagon, pancreatic protein and polypeptide hormones respectively, which have been studied in great detail.
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PMID:Purification, crystallisation and preliminary X-ray studies on avian pancreatic polypeptide. 91 91

In experiments with rabbits, glucagon prolonged the half-period of absorption of sodium iodide 125J in the left ventricular myocardium. Regitine prevented acceleration of the heart rate and impairment of capillary flow after glucagon. In healthy rabbits hippurate 125J clearance was unaffected by glucagon. After injury of the heart muscle by injection of silver nitrate solution into the left ventricular wall and depression of blood pressure, glucagon partly normalized renal clearance of hippurate 125J.
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PMID:The influence of glucagon on the blood supply of the heart and kidneys in rabbits. 121 13

We hypothesized the existence of vagal arginine sensors in the liver which modulate arginine-induced pancreatic hormone secretion. The present study was carried out to examine the efferent pathways and receptor mechanisms from arginine sensors using selective vagotomies and autonomic drugs on the secretion of insulin and glucagon after ip injection of L-arginine (1 g/kg BW) in rats in an unanesthetized and unrestrained state. Hepatic vagotomy (sectioning of the hepatic branch of the vagus nerve) enhanced both plasma insulin and glucagon concentrations after ip arginine more than those in sham-vagotomized (control) rats. The effect of hepatic vagotomy was blocked by adding celiac vagotomy (sectioning of the celiac branches of the vagus nerve) or by previous administration of atropine methyl nitrate (10 mg/kg BW), but not by phentolamine (1 mg/kg BW) or propranolol (2 mg/kg BW). Celiac vagotomy alone did not affect the plasma insulin concentration; however, it reduced the plasma glucagon concentration after ip arginine compared to that in sham-vagotomized rats. Administration of atropine alone did not affect plasma insulin or glucagon concentrations after ip arginine. These results suggest that celiac branches of the vagus nerve act as efferent pathways to the pancreas through a muscarinic receptor mechanism in the hepatic arginine sensor-mediated pancreatic neuroendocrine system. The physiological role of these hepatic sensors may be to prevent arginine-induced exaggerated pancreatic hormone secretion and maintain blood glucose homeostasis.
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PMID:Modulation of arginine-induced insulin and glucagon secretion by the hepatic vagus nerve in the rat: effects of celiac vagotomy and administration of atropine. 220 80

Vasoactive intestinal peptide (VIP) has been shown to stimulate adenylate cyclase activity in plasma membranes isolated from canine renal cortex, outer and inner medulla in vitro. Though related hormones such as glucagon also stimulate adenylate cyclase in these membrane preparations, it is likely that VIP interacts with specific VIP receptors since the VIP receptor antagonist, (4Cl-D-Phe6, Leu17)-VIP, is capable of reducing the response to VIP, but not that to glucagon. Also binding of 125I-VIP to cortical renal plasma membranes shows competition by unlabelled VIP, but not by glucagon. Strain 1 (and clone CL(8)1b cells derived from the established cultured dog kidney cell line, MDCK, have been shown also to respond selectively to VIP by an increase in adenylate cyclase activity and cyclic AMP accumulation in intact cells. A physiological correlate of VIP activation of adenylate cyclase has been sought by addition of VIP to reconstituted epithelial monolayers of strain 1 MDCK cells clamped in Ussing chambers. VIP addition to the basal-lateral cell aspects generates an inward short-circuit current that is sensitive to replacement of medium Cl- by NO3-, and to inhibition by the Cl- channel blocker, 3-nitro-2(3-phenylpropylamino)-benzoic acid, consistent with VIP stimulation of transepithelial Cl- secretion.
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PMID:Vasoactive intestinal peptide control of renal adenylate cyclase: in vitro studies of canine renal membranes and cultured canine renal epithelial (MDCK) cells. 254 73

To determine the mechanism of time-dependent hyperglycemia due to intracranial injection of 2-deoxy-D-glucose (2DG), we examined the effects of various blockers of the autonomic nervous system on the hyperglycemia and hyperglucagonemia induced by intracranial injection of 2DG in male Wistar rats in light and dark periods. Hexamethonium inhibited the hyperglycemia in both light and dark periods but did not block the hyperglucagonemia in either period. Intracranial injection of 2DG did not affect the plasma insulin concentration in saline-treated control rats, but hexamethonium caused an increase in the basal plasma insulin concentration and further increase in the plasma concentration after 2DG injection in the light period. Phenoxybenzamine, an alpha-adrenergic blocker, inhibited the hyperglycemia only in the light period and the hyperglucagonemia only in the dark period and slightly stimulated the basal concentrations of insulin and glucagon only in the light period. Propranolol, a beta-adrenergic blocker, blocked the hyperglycemia and hyperglucagonemia and also lowered the basal plasma glucagon concentration in both periods. Atropine sulfate and atropine methyl nitrate, muscarinic blockers, inhibited hyperglycemia only in the light and dark period, respectively. In contrast, both drugs blocked the hyperglucagonemia in both periods. These findings suggest that the autonomic nervous system is involved time dependently in the hyperglycemia and hyperglucagonemia due to intracranial 2DG injection.
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PMID:Time-dependent involvement of autonomic nervous system in hyperglycemia due to 2-deoxy-D-glucose. 290 68

Glutathione (GSH) is released into hepatic sinusoids by a carrier-mediated process. The importance of transmembrane potential difference (PD) as a driving force for hepatic efflux of GSH from isolated perfused rat liver was investigated. The membrane PD was measured using intracellular microelectrodes as PD was altered over the physiological range by ion substitution in the perfusate. The effect of a change in membrane PD on the rate of efflux of GSH into the perfusate was determined. Because GSH carries a net negative charge at physiological values of pH, we predicted that hyperpolarization of cells would increase efflux, whereas depolarization would decrease efflux. Three different manipulations were used to depolarize the hepatocyte membrane to a similar degree, and variable effects on GSH efflux were observed. Substitution of Cl with gluconate in the perfusate depolarized the hepatocyte but had no effect on GSH efflux, whereas substitution of Na with choline in the perfusate increased GSH efflux to 110% of basal values. Perfusion with K+ inhibited GSH efflux by 21%. The latter two manipulations were associated with evidence of hepatic injury. Hyperpolarization of the hepatocyte also had variable effects on GSH efflux. Substitution of Cl with nitrate in the perfusate transiently increased the membrane PD and decreased GSH efflux, whereas perfusion with glucagon caused a sustained increase in membrane PD but did not alter GSH efflux rates. None of the latter manipulations was associated with hepatic injury and thus no consistent relationship between membrane PD and sinusoidal efflux of GSH was demonstrated. We conclude that in the isolated perfused rat liver, efflux of GSH is not driven directly by membrane PD.
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PMID:Hepatic efflux of glutathione by the perfused rat liver: role of membrane potential difference. 318 47

Non-transferrin-bound iron is efficiently cleared from serum by the liver and may be primarily responsible for the hepatic damage seen in iron-overload states. We tested the hypothesis that transport of ionic iron is driven by the negative electrical potential difference across the liver cell membrane. Extraction of 55Fe-labeled ferrous iron (1 microM) from Krebs bicarbonate buffer by the perfused rat liver was continuously monitored as the transmembrane potential difference (measured using conventional microelectrodes) was altered over the physiologic range by isosmotic ion substitution. Resting membrane potential in Krebs bicarbonate buffer was -28 +/- 1 mV. Perfusion with 1 microM ferrous iron caused a reversible 3 +/- 1 mV depolarization, and higher concentrations of iron caused even greater depolarization. Conversely, depolarization of the liver cells consistently reduced iron extraction. Replacement of sodium with potassium (70 mM) or choline (131 mM) depolarized the hepatocytes to -15 and -20 mV and decreased iron extraction by 28 and 31%, respectively. Perfusion with bicarbonate-free solutions containing tricine buffer (10 mM) reduced the membrane potential to -23 mV and reduced iron extraction by 18%. In contrast, the high basal extraction of iron (91.1 +/- 1.4%) was not further increased by substitution of nitrate for chloride (-46 mV) or infusion of glucagon (-34 mV). All effects were reversible, suggesting that perfusion with 1 microM iron produced little toxicity. These findings are consistent with an electrogenic transport mechanism for uptake of non-transferrin-bound iron that is driven by the transmembrane potential difference.
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PMID:Non-transferrin-bound iron uptake by rat liver. Role of membrane potential difference. 333 96

Bouin-fixed tissues from non-diabetic adult human pancreata display an argyrophil reaction mainly in the periphery of the islets with the silver technique of Sevier-Munger. The nature of these argyrophil cells was examined after restaining by an indirect immunocytochemical method using antibodies against insulin, glucagon, somatostatin and pancreatic polypeptide. After this procedure the argyrophil cells were identified as glucagon (A-) cells and pancreatic polypeptide (PP-) cells, although the latter exhibited a weaker reaction. The insulin (B-) cells and somatostatin (D-) cells were unreactive. The results show that the Seiver-Munger stain is of equal value to the Grimelius silver nitrate stain in adult human pancreatic islets after fixation in Bouin's fluid.
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PMID:Immunocytochemical study of argyrophil (Sevier Munger) endocrine cells of adult human pancreas. 610 8

Hepatocytes isolated from livers of rats with various models of acute uremia (binephrectomy, ureter ligation, uranyl nitrate-induced, or ischemic ARF) were incubated with glucagon, adrenalin, or cyclic AMP using serine as a substrate. A marked increase in glucose production was observed in the hepatocytes of uranyl nitrate-treated, binephrectomized, and ureter-ligated rats compared to starved controls or sham-operated animals. This effect was strengthened in the presence of glucagon, adrenaline, or cyclic AMP. In liver cells of binephrectomized and ureter-ligated animals, the production of acetoacetate and beta-hydroxybutyrate was significantly higher than in controls and sham-operated rats. Oxoglutarate and ATP production was only enhanced after ureter ligation. The correlation between glucose concentration and the cytosolic redox state was different in control and sham-operated rats than in either uremic group. This study confirms earlier investigations of a key role of serine in carbohydrate metabolism in acutely uremic rats.
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PMID:Effect of serine on gluconeogenic ability of hepatocytes in acute uremia. 633 Apr 26


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