Direct Effect of Cortisol and Cortisone on Insulin and Glucagon Secretion*

Abstract

The direct effects of cortisol and cortisone on insulin and glucagon secretion by the isolated perfused rat pancreas were examined. Cortisone, but not cortisol, in a final concentration of 10(-4) M acutely and strongly inhibited both phases of glucose- and arginine-induced insulin secretion. In repeated pulse administrations, the second infusion of cortisone elicited an inhibition of insulin release equal to the first response. Glucagon output was slightly suppressed by cortisol and more significantly by cortisone in a glucose-free medium. The blockade of alpha-adrenergic receptors by phentolamine attenuated, but did not prevent, the strong inhibitory action of cortisone on insulin secretion.

Glikokortykosteroidy a czynność komórek beta

“…However, such investigations have also produced conflicting results, probably because of various study designs, GC preparations used, dosages, and time of exposure, as well as different characteristics of the studied cells. The majority of studies indicate an inhibitory GC effect on insulin secretion in vitro [50][51][52][53][54][55][56]. The effect is dosedependent and abolished by addition of GR antagonist RU486 to the cell culture [47,[56][57][58][59][60].…”

“…On the contrary, GCs do not seem to alter basal insulin secretion in vitro [52,56]. Some studies indicate a rapid GC inhibitory effect [50,51], whereas others demonstrate a delayed onset response [52,54,56]. Additionally, prior exposure to DEX attenuates beta cell reaction to other insulin secretagogues, such as potassium, arginine, tolbutamide, and 12-O-tetradeacanoyl phorbol-13-actetate (TPA) [50,56,59].…”

“…Some studies indicate a rapid GC inhibitory effect [50,51], whereas others demonstrate a delayed onset response [52,54,56]. Additionally, prior exposure to DEX attenuates beta cell reaction to other insulin secretagogues, such as potassium, arginine, tolbutamide, and 12-O-tetradeacanoyl phorbol-13-actetate (TPA) [50,56,59]. In contrast, isolated islets from the DEX-pretreated rats displayed increased GSIS -perhaps reflecting a rapid compensatory adaptation to insulin resistance, while primary islet cultures from the same strain without prior GCs exposure presented attenuated insulin response to glucose when DEX was added to the culture medium [44].…”

“…Jakkolwiek tego typu analizy również dostarczały sprzecznych wyników, prawdopodobnie z powodu różnych projektów badania, stosowanych preparatów GKS, dawek i czasu eskpozycji, jak również odmiennych cech użytych komórek. W większości badań wykazano jednak hamujące działanie GKS na wydzielanie insuliny in vitro [50][51][52][53][54][55][56]. Efekt ten jest zależny od dawki i znoszony przez dodanie RU486 -antagonisty GR, do hodowli komórek [47,[56][57][58][59][60].…”

“…Nie wydają się jednak wpływać na podstawowe wydzielanie insuliny in vitro [52,56]. Wyniki niektórych badań wykazują szybki efekt hamujący GKS [50,51], podczas gdy inne sugerują raczej odpowiedź o opóźnionym początku [52,54,56].…”