Summary
Previous experiments have shown that in an oral glucose tolerance test insulin is mobilized in the first phase independent of the following hyperglycemia. By giving different amounts of glucose (0.5–2.0 g/kg) in conscious trained dogs it was shown that this early phase of insulin secretion was stimulated independently of the administered glucose load by additional mechanisms. These mechanisms, at least partly, were triggered in the nerve endings of the cavity of mouth: their paralysis by mucosal anaesthesia abolished the early IRI-increase in intact animals as well as after feeding glucose to dogs bearing oesophagus fistulas. Spraying sodium cyclamate into the mouth did not produce any IRI-increase. The results indicate that the taste modality “sweet” is not involved in this reflex response. Conditioned reflexes as a consequence of the training programme or of the daily feeding regime were excluded by control experiments.
Résumé
Des expériences préalables ont montré que dans un test oral de tolérance au glucose l'insuline est mobilisée au cours de la première phase indépendamment de l'hyperglycémie qui suit. Si l'on administre différentes doses de glucose (0.5–2.0 g/kg) à des chiens éveillés et entrainés, il apparaît que cette première phase de la sécrétion d'insuline est stimulée par des mécanismes additifs indépendamment de la charge de glucose appliquée. Ces mécanismes, au moins en partie, commencent aux terminaisons nerveuses de la cavité buccale: leur paralysie par anesthésie de la muqueuse empêche la première augmentation réflexe d'IRI chez les animaux intacts de même que l'augmentation d'IRI après alimentation simulée de glucose chez des chiens ayant des fistules de l'oesophage. Le fait de pulvériser du cyclamate de sodium dans la cavité buccale ne provoque aucune augmentation d'IRI. Cela signifie que la saveur “sucrée” n'intervient pas dans le mécanisme du réflexe. Les mécanismes des réflexes conditionnés qui sont la conséquence d'un programme d'entraînement ou d'un régime alimentaire journalier étaient exclus par des expériences de contrôle.
Zusammenfassung
Vorangegangene Experimente hatten ergeben, daß bei einem oralen Glucosetoleranztest in einer ersten Phase Insulin unabhängig von der erst darauffolgenden Hyperglykämie freigesetzt wird. Durch Gabe unterschiedlicher Glucosedosen (0.5–2.0 g/kg) an wache, trainierte Schäferhunde wird in dieser Mitteilung gezeigt, daß diese erste Phase der Insulinsekretion von der verabfolgten Glucosedosis unabhängig durch zusätzliche Mechanismen stimuliert wird. Diese Mechanismen beginnen zumindest teilweise in Nervenendigungen der Mundhöhle: ihre Betäubung durch Schleimhautanästhesie verhindert den frühzeitigen reflektorischen IRI-Anstieg bei intakten Tieren sowie den gleichen reflektorischen IRI-Anstieg nach Glucosescheinfütterung an Hunde mit Oesophagusfisteln. Einstäuben von Natrium-Zyklamat in die Mundhöhle ruft keinen IRI-Anstieg hervor. Die Geschmacksrichtung „süß” ist also nicht an den reflektorischen Mechanismen beteiligt. Bedingt-reflektorische Vorgänge als Folge des Trainingsprogramms oder der täglichen Nahrungsaufnahme wurden durch Kontrollversuche ausgeschlossen.
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The authors are grateful to Mrs. Karla Brüllke, Mrs. Helga Schröder, Miss Gisela Schmidt and Miss Helga Schüler for careful technical assistance.
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Fischer, U., Hommel, H., Ziegler, M. et al. The mechanism of insulin secretion after oral glucose administration. Diabetologia 8, 385–390 (1972). https://doi.org/10.1007/BF01212164
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DOI: https://doi.org/10.1007/BF01212164