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Factors controlling insulin secretion in vitro

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Riassunto

Il progresso delle tecniche per la conservazione delle isole pancreatichein vitro ha reso possibile lo studio dell'effetto diretto di diversi agenti e delle variazioni metaboliche sulla funzione delle cellule β. Il glucosio deve essere metabolizzato all'interno della cellula β per dare il via alla secrezione di insulina: l'importanza del ciclo di Krebs è suggerita dai risultati sperimentali. Il glucosio stimola anche la sintesi di insulina, ma indipendentemente dalla secrezione di insulina. L'ormone dell'accrescimento ed il lattogeno placentare potenziano entrambi i processi, probabilmente facilitando la scissione metabolica del glucosio. Il ruolo delle catecolamine e del glucagone nella regolazione della secrezione di insulina è stato definito negli ultimi anni.

Resume

Le progrès des techniques de conservation des îles pancréatiquesin vitro a donné la possibilité d'étudier l'effet direct de plusieurs agents et des variations métaboliques sur la fonction des cellules-β. Le glucose doit être métabolisé à l'intérieur de la cellule-β pour avoir la sécrétion d'insuline: l'importance du cycle du Krebs est suggerée par les résultats expérimentaux. Le glucose stimule aussi la synthèse de l'insuline, mais d'une façon indépendante de la sécrétion d'insuline. L'hormone somatotrope et le lactogène placentaire augmentent les deux procès, probablement en facilitant la scission métabolique du glucose. Le rôle des catécholamines et du glucagone dans la régulation de la sécrétion d'insuline a été défini dans les dernières années.

Resumen

El progreso de las técnicas de conservación de islas pancreáticasin vitro, ha hecho posible el estudio del efecto directo de varios agentes y de las variaciones metabólicas sobre la función de las células β. La glucosa debe ser metabolizada en la célula β para que pueda comenzar la secreción de insulina; la importancia del ciclo de Krebs está confirmada por los resultados experimentales. La glucosa estimula inclusive la síntesis de insulina, pero independientemente de la secreción de insulina. La hormona del crecimiento y el lactógeno placentar potencian ambos procesos, probablemente facilitando la escisión metabólica de la glucosa. El papel de las catecolaminas y del glucagón en la regulación de la secreción de insulina ha sido definido durante estos últimos años.

Zusammenfassung

Der Fortschritt in den Erhaltungstechniken von Pankreas-Inselnin vitro ermoeglichte die Untersuchung des direkten Effektes von verschiedenen Agentien sowie der metabolischen Veränderungen in der Funktion der β-Zellen. Die Glukose muss innerhalb der β-Zelle metabolisiert werden, um die Insulinsekretion einzuleiten. Die Bedeutung des Krebs'schen Zyklus wird durch die experimentellen Resultate gestuetzt. Die Glukose foerdert auch die Insulin-Synthese, aber unabhaengig von der Insulin-Sekretion. Das Wachstumshormon sowie das Plazentarlactogen verstaerken beide Prozesse, indem sie wahrscheinlich die metabolische Spaltung der Glukose erleichtern. Die Rolle der Katecholamine und des Glukagons in der Regulierung der Insulinsekretion wurde in den letzten Jahren bestimmt.

Summary

The development of techniques for maintaining pancreatic isletsin vitro has made it feasible to study the direct effect of various agents and metabolic changes on β-cell function. Glucose has to be metabolized within the β-cell to provide the signal for insulin secretion, and the importance of the Krebs' cycle is suggested by experimental results. Glucose also stimulates insulin synthesis, but independently from insulin secretion. Growth hormone and placental lactogen enhance both processes, possibly by facilitating the metabolic breakdown of glucose. The role of catecholamines and glucagon in the regulation of insulin secretion has been defined during the past few years.

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Original material included in this review resulted from work supported by Grant MT-1202, Medical Research Council of Canada, and by funds of the Hospital for Sick Children.

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Martin, J.M. Factors controlling insulin secretion in vitro. Acta diabet. lat 6, 689–712 (1969). https://doi.org/10.1007/BF01548082

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