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  • 1970-1974  (2)
  • Autoradiography  (1)
  • insulin release  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 7 (1971), S. 339-348 
    ISSN: 1432-0428
    Keywords: Autoradiography ; 5-hydroxytryptamine ; 5-hydroxytryptophan ; monoamine oxidase inhibition ; mouse ; pancreatic islets ; reserpine ; ultrastructure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé En appliquant la technique autoradiographique, on a étudié la distribution cellulaire et subcellulaire de la radioactivité dans les îlots pancréatiques de la souris après une injection intra-veineuse de3H-5-hydroxytryptophane. Des grains d'argent autoradiographiques dont la plupart représentent probablement de la 5-hydroxytryptamine qui s'est formée à partir du précurseur marqué, sont apparus sur les cellules A2 et B, tandis que très peu de grains ont été trouvés sur les cellules A1 à chacun des examens (entre 20 min et 16 h) et de même après l'inhibition de la monoamine-oxidase. L'analyse quantitative des coupes autoradiographiques a révélé que la concentration de grains d'argent sur les granules spécifiques des cellules A2 et B était 5 à 10 fois plus élevée que sur les parties restantes de ces cellules. Sur les cellules A2 le nombre le plus élevé de grains a été noté 20 min après l'injection du marqueur et sur les cellules B une heure après cette injection. Au bout de 8 h, il n'apparaissait que très peu de grains d'argent sur les cellules des îlots, et plus aucun au bout de 16 h. L'inhibition de la monoamine-oxidase a provoqué une augmentation de la rétention de marqueur sur les cellules des îlots, plus prononcée sur les cellules A2. Un traitement préalable à la réserpine a supprimé cette réaction autoradiographique.
    Abstract: Zusammenfassung Mit Hilfe der Technik der Autoradiographie wurde die zelluläre und subzelluläre Verteilung der Radioaktivität nach intravenöser Applikation von3H-5-Hydroxytryptophan in den Pankreasinseln der Maus untersucht. Die autoradiographischen Silberkörner, welche zumeist 5-Hydroxytryptamin darstellen, das aus der radioaktiven Ausgangssubstanz gebildet worden war, erschienen über den A2 und B-Zellen, während nach jedem untersuchten Zeitintervall (20 min–16 Std) auch wenn die Monoamino-Oxidase gehemmt wurde, nur sehr wenige Körner über den A1-Zellen erschienen. Quantitative Untersuchungen der Autoradiographieschnitte zeigten, daß die Konzentration der Silberkörner über den spezifischen Granula der A2-Zellen und der B-Zellen etwa 5–10 mal höher als über den restlichen Teilen der Zellen war. In den A2-Zellen wurde die höchste Körnerkonzentration nach 20 min, in den B-Zellen 1 Std nach Injektion der markierten Substanz festgestellt. Nach 8 Std zeigten sich nur wenige, nach 16 Std keine Silberkörner mehr über den Inselzellen. Die Hemmung der Monoamino-Oxidase verursachte eine vermehrte Anreicherung von Radioaktivität über den Inselzellen, am meisten über den A2-Zellen. Eine Vorbehandlung mit Reserpin verhinderte die autoradiographische Darstellung.
    Notes: Summary By application of autoradiographic technique the cellular and subcellular distribution of radio-activity in mouse pancreatic islets was investigated following intravenous administration of3H-5-hydroxytryptophan. Autoradiographic silver grains, most of which probably represent 5-hydroxytryptamine formed from the labelled precursor, appeared over A2 and B cells, whereas very few grains were recorded over A1 cells at any time investigated (20 min–16 hours) and also when monoamine oxidase was inhibited. Quantitative analysis of autoradiographic sections revealed that the concentration of silver grains over the specific granules of A2 and B cells was 5–10 times higher than over the remaining parts of these cells. In A2 cells the highest grain count was recorded at 20 minutes, in B cells at 1 hour after the injection of label. After 8 hours very few, and after 16 hours no silver grains appeared over islet cells. Inhibition of monoamine oxidase caused an increased retention of label over islet cells, most pronounced over A2 cells. Pretreatment with reserpine abolished the autoradiographic reaction.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 10 (1974), S. 717-724 
    ISSN: 1432-0428
    Keywords: Acid amyloglucosidase ; insulin release ; plasma immunoreactive insulin ; sulphonylurea derivatives ; α-amylase ; β-glucuronidase ; albumin ; isopropylnoradrenaline ; arginine ; isobutylmethylxanthine ; secretin ; mice ; rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of exogenous acid amyloglucosidase on sulphonylurea-induced insulin release was investigated in mice and rats. 1. Pretreatment of mice with acid amyloglucosidase enhanced insulin release induced by the different sulphonylurea derivatives, carbutamide, tolbutamide, glibenclamide, and glibornuride. 2. A dose-response relationship between glibenclamide-induced insulin response and amyloglucosidase dosage covering a 64-fold concentration range was established in mice. 3. Pretreatment of the animals with other macromolecules of similar physiological or chemical properties to acid amyloglucosidase such asα-amylase,β-glucuronidase and albumin did not influence glibenlamide-induced insulin release. 4. The effect of acid amyloglucosidase pretreatment on insulin release induced by different agents known to affect the islet-cell adenylate cyclase-cyclic AMP system such as secretin, L-isopropylnoradrenaline (L-IPNA), arginine, glibenclamide and 3-isobutyl-1-methylxanthine (IBMX) was tested. It was observed that in animals pretreated with acid amyloglucosidase, insulin release was enhanced when stimulated by glibenclamide, a phosphodiesterase inhibitor, but it was similarly enhanced by arginine, a phosphodiesterase activator. Insulin release induced by secretin, L-IPNA, and IBMX was unaffected. 5. Acid amyloglucosidase pretreatment in rats enhanced plasma immunoreactive insulin levels following glibenclamide injection not only in the peripheral veins but also in the portal vein. 6. Mice fasted for 24 hrs displayed a markedly depressed insulin response to tolbutamide injection. Pretreatment of the fasted animals with acid amyloglucosidase could restore the tolbutamide-induced insulin release to the same level as that recorded in a group of freely fed mice. It is suggested that acid amyloglucosidase plays an important role in insulin secretion induced by sulphonylureas. Most evidence suggests that this effect is exerted within the B-cell although an additional effect on the liver cannot be ruled out.
    Type of Medium: Electronic Resource
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