Effect of Endogenous Insulin on Pancreatic Exocrine Secretion in Perfused Dog Pancreas

Lee, K Y; Krusch, David A.; Zhou, Luxian; Song, Young Duk; Chang, Tsun-Hou; Wy, Chey

doi:10.1097/00006676-199508000-00013

Cited by 16 publications

(10 citation statements)

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“…The infusion of anti-insulin serum also resulted in elevation of SS in portal venous effluent, and the inhibition of PES by the anti-insulin serum was partially reversed by co-infusion of an anti-SS serum [10]. The same effects of anti-insulin serum were observed in isolated and perfused canine pancreata [111]. In addition to SS, PP was also elevated in the portal effluent by the anti-insulin serum.…”

Section: Endocrine-exocrine Axis Of the Pancreasmentioning

confidence: 55%

Neural hormonal regulation of exocrine pancreatic secretion

Chey¹,

Chang²

2001

Pancreatology

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Section: Endocrine-exocrine Axis Of the Pancreasmentioning

confidence: 55%

Neural hormonal regulation of exocrine pancreatic secretion

Chey¹,

Chang²

2001

Pancreatology

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“…Coinfusion of the two gut hormones with the anti-insulin serum resulted in an elevation of SS and pancreatic polypeptide in the portal venous effluent. Coinfusion with the anti-insulin serum together with an anti-SS serum, however, restored secretin, and CCK stimulated pancreatic secretion of fluid and bicarbonate (15,16), thereby suggesting that endogenous SS from the pancreas plays a negative regulatory role in pancreatic exocrine secretion. Thus it is very likely that MEK inhibits pancreatic secretion through stimulation of SS release from the pancreatic islet.…”

Section: Discussionmentioning

confidence: 99%

MEK inhibits secretin release and pancreatic secretion: roles of secretin-releasing peptide and somatostatin

Lee

Chang

et al. 2001

American Journal of Physiology-Gastrointestinal and Liver Physi

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We investigated the mechanism of action of methionine enkephalin (MEK) on HCl-stimulated secretin release and pancreatic exocrine secretion. Anesthetized rats with pancreatobiliary cannulas and isolated upper small intestinal loops were perfused intraduodenally with 0.01 N HCl while bile and pancreatic juice were diverted. The effect of intravenous MEK on acid-stimulated secretin release and pancreatic exocrine secretion was then studied with or without coinfusion of naloxone, an anti-somatostatin (SS) serum, or normal rabbit serum. Duodenal acid perfusate, which contains secretin-releasing peptide (SRP) activity, was collected from donor rats with or without pretreatment with MEK, MEK + naloxone, or MEK + anti-SS serum, concentrated by ultrafiltration, and neutralized. The concentrated acid perfusate (CAP), which contains SRP bioactivity, was infused intraduodenally into recipient rats. MEK increased plasma SS concentration and inhibited secretin release and pancreatic fluid and bicarbonate secretion dose-dependently. The inhibition was partially reversed by naloxone and anti-SS serum but not by normal rabbit serum. In recipient rats, CAP increased plasma secretin level and pancreatic secretion. CAP SRP bioactivity decreased when it was collected from MEK-treated donor rats; this was partially reversed by coinfusion with naloxone or anti-SS serum. These results suggest that in the rat, MEK inhibition of acid-stimulated pancreatic secretion and secretin release involves suppression of SRP activity release. Thus the MEK inhibitory effect appears to be mediated in part by endogenous SS.

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“…Ferrer et al [23] reported that exogenous insulin increased pancreatic juice flow and decreased amylase activity in the basal state in vivo in rats. On the other hand, although the results in dispersed acinar cells or isolated perfused pancreas preparations may be influenced in part by preparation artifacts, most of them [8,10,16,17,24,25] showed a potentiating effect of insulin on pancreatic amylase secretion in rats and dogs. Recently, the effect of insulin and glucose on pancreatic secretion in humans has been reported by Lam et al [18].…”

Section: Discussionmentioning

confidence: 99%

“…Matsushita et al [25] showed a direct effect of insulin on pancreatic acinar cells that is mediated by increasing Na + , K + -ATPase activity. In addition, it has been reported that immunoneutralization of circulating insulin resulted in increase in local release of somatostatin and pancreatic polypeptide (PP) in the perfused dog pancreas [10]. Both somatostatin and PP are well known to inhibit pancreatic exocrine secretion.…”

Section: Discussionmentioning

confidence: 99%

“…In fact, both exogenous and endogenous insulin has been reported to potentiate cholecystokinin (CCK)-induced pancreatic secretion in isolated and the perfused rat pancreas [8]. In addition, Lee et al reported that immunoneutralization with anti-insulin serum completely blocks pancreatic exocrine secretion stimulated by secretin and CCK in conscious rats [9] and the isolated perfused rat pancreas [10]. These results indicate that insulin may influence the stimulation of pancreatic secretion by CCK.…”

Section: Introductionmentioning

confidence: 99%

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