The potentiating influences of insulin on pancreozymin‐induced hyperpolarization and amylase release in the pancreatic acinar cell.

Abstract

SUMARY1. Insulin (1 u./ml.) potentiated the release of amylase from isolated pancreas of rats perfused with erythrocyte-containing medium and stimulated by 0-5 m-u. pancreozymin (Pz)/ml., whereas the same concentration of insulin failed to potentiate the response evoked by 5 or 200 m-u. Pz/ml.2. Intracellular measurement of membrane potentials from the acinar cells of the same preparations showed that insulin (1 u./ml.) simultaneously potentiates the hyperpolarization and amylase release in response to 0-5 rn-u. Pz/ml.3. These effects of insulin on the Pz-induced responses were inhibited by ouabain (3 x 105 M).4. The results suggest that insulin, in the concentration studied, has a potentiating action on the activity of an electrogenic Na pump, which maintains the hyperpolarization and amylase release during continuous stimulation with Pz.5. Insulin also potentiated the Pz-induced amylase release in the rat pancreata in situ after vagotomy and ligature of the pyloric region.

Microcirculatory Patterns in Human Pancreas: Supplementary Observations of Vascular Casts by Scanning Electron Microscopy.

“…el Lobular capillaries replicated via the acinar artery. X 230 (KANNO and SAITO, 1976). Possible effects of bioactive substances released from the islets and distributed to the exocrine pancreas have been reviewed by FUJITA et al (1981) and by WILLIAMS and GOLDFINE (1993).…”

Microvasculature as studied by the microvascular corrosion casting/scanning electron microscope method. I. Endocrine and digestive system.

“…Evidence favoring this view has accumulated: insulin potentiates the effect of pancreozymin upon the exocrine pancreas (KANNO and SAITO, 1976); injection of glucagon causes degranulation of exocrine cells (SALTER, DAVIDSON and BEST, 1957); somatostatin inhibits the pancreatic enzyme secretion stimulated by cholecystokinin (DOLLINGER et al, 1976); and pancreatic polypeptide inhibits the secretion and cholecystokinin effect upon the exocine pancreas (Lin et al, 1977).…”

Interaction of Islet Hormones with Cholecystokinin Octapeptide‐Evoked Secretory Responses in the Isolated Pancreas of Normal and Diabetic Rats

“…In previous studies, it was demonstrated that the pancreatic islet hormones, especially Ins at concentrations employed in this study, had only little secretory effect on the exocrine pancreas (Couture et al 1972;Kayasseh et al 1979;Singh, 1985b;Chey, 1993) but it markedly enhanced the secretory responses to ACh and CCK-8 (Kanno & Saito, 1976;Saito et al 1980a,b;Singh, 1985b;Williams & Goldfine, 1993;Owyang, 1993). In agreement with these previous studies our present results have also confirmed these interesting findings.…”

“…Previous studies have shown that Ins alone has very little effect on pancreatic amylase secretion (Couture et al 1972;Singh, 1985b) but it can markedly enhance the secretory response to ACh and CCK-8 (Kanno & Saito, 1976;Saito et al 1980a,b;Singh, 1985b). This potentiatory action of Ins on ACh-evoked enzyme secretion is believed to be associated with the mobilization of cellular Ca¥ and cAMP metabolism (Singh, 1983(Singh, , 1985bJuma et al 1997a) and zymogen granular regulatory protein phosphorylation (Burnham & Williams, 1982;Williams & Goldfine, 1993).…”