Glucose-Dependent Insulinotropic Action of Cholecystokinin and Caerulein in the Isolated Perfused Rat Pancreas

Sakamoto, Choitsu; Ōtsuki, Makoto; Ohki, Atsushi; Yuu, Hosai; Maeda, Mitsuo; Yamasaki, Tohru; Baba, Shigeaki

doi:10.1210/endo-110-2-398

Cited by 52 publications

(22 citation statements)

References 23 publications

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“…Increase in release from the NIL is a distinct possibility, at least for cholecystokinin, which is coreleased with vasopres sin [12] and fordynorphin, which is altered in content in the same way as vasopressin [35], because hyperosmolality in diabetes will un doubtedly lead to an increase in vasopressin release [33], If there is indeed an increase in the release of dynorphin and cholecystokinin from the NIL, the increased secretion of these neuropeptides and P-endorphin may stimu late insulin secretion from the 'residual' pan creatic islets in streptozotocin-treated rats, as a compensatory mechanism for the decrease in insulin secretion. Opioid peptides [36] and cholecystokinin [37] have been shown to be insulinotropic when administered peripher ally. The increase in p-endorphin release from the pituitary could be the result of increased adrenergic stimulation [38],…”

Section: Discussionmentioning

confidence: 99%

Pituitary Contents of Beta-Endorphin, Dynorphin, Substance P, Cholecystokinin and Somatostatin in Rats with Streptozotocin-lnduced Diabetes

Tang¹,

Wong²

1996

Neurosignals

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The effects of streptozotocin-induced diabetes on pituitary neuropeptides were studied. Substance P, dynorphin and β-endorphin in both pituitary lobes and cholecystokinin and somatostatin in the neurointermediate lobe () were measured 4 weeks after streptozotocin treatment in adult male rats. There were significant decreases of substance P levels in both the anterior lobe (AL) and , and of cholecystokinin, dynorphin and β-endorphin in the , whereas the dynorphin content in the AL increased, when values were expressed on a per-lobe basis. On a per-milligram-protein basis, however, only β-endorphin in the showed a significant decrease, while AL β-endorphin and dynorphin were increased. Correlated with these changes were a drastic decrease in the serum insulin level and a marked increase in serum glucose and corticosterone levels. All these changes were reversible with insulin treatment. It is suggested that the decrease in contents of neuropeptides demonstrated (except for β-endorphin) might be due to mechanisms other than a change in synthesis.

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Section: Discussionmentioning

confidence: 99%

Pituitary Contents of Beta-Endorphin, Dynorphin, Substance P, Cholecystokinin and Somatostatin in Rats with Streptozotocin-lnduced Diabetes

Tang¹,

Wong²

1996

Neurosignals

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“…In subsequent studies, Otsuki's group further demonstrated that CCK-and cerulein-induced insulin secretion is dependent on the glucose concentration ( Fig. 4) (20). Otsuki et al (19)(20)(21)(22) published a number of articles describing this perfusion system.…”

Section: Discussionmentioning

confidence: 98%

Exocrine Pancreatic Physiology

Ogami

Ōtsuki²

1998

Pancreas

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Japanese researchers have contributed to the development of various areas of pancreatic physiology such as hormonal and neural regulation of pancreatic exocrine secretion, effect of nutrients on the exocrine pancreas, and stimulus-secretion coupling in the exocrine pancreas. Among them, we selected three fruitful areas and reviewed them. These are in vitro experiment with the perfusion of the isolated rat pancreas, research related to the cholecystokinin (CCK)-releasing factor of pancreatic acinar cell origin (monitor peptide), and development and characterization of two genetically diabetic rats: WBN/Kob and OLETF (Otsuka Long-Evans Tokushima fatty) rats. PERFUSION OF ISOLATED PANCREASKanno (1) developed an elegant and fine method of perfusion of the rat isolated pancreas. In his study, the inlet of the vascular perfusion was the superior mesenteric artery, and the outlet was the portal vein. The common duct was constantly flushed. The inlet of perfusion of the common duct was the hepatic end of the duct, and the outlet was the duodenal end. This method was further modified to allow more effective perfusion of the vascuSummary: Exocrine pancreatic physiology has been actively investigated in Japan during the past 30 years. We selected three areas and reviewed them for this article. The selected areas are perfusion of the isolated pancreas, cholecystokinin (CCK)-releasing factor from pancreatic juice (monitor peptide), ~ 265 and genetically diabetic rats. The aim of this article is to present a brief overview of the selected areas of exocrine pancreatic physiology in Japan so that future research can be productively directed. Key Words: Exocrine pancreatic physiologyCholecystokinin-releasing factor-Genetically diabetic rats. lar system and simultaneous measuring of the flow rate of pancreatic juice ( 2 ) . The inlets of vascular perfusion were both the superior mesenteric artery and the celiac artery, whereas the outlet was the portal vein. During part of the experiment, the hepatic end of the common duct was ligated, and the pancreatic juice collected from the duodenal end after cannulation with a stainless steel tube (Fig. 1). By using this system of perfusion of the isolated pancreas, Kanno et al.(3) demonstrated that addition of exogenous insulin to the perfusate potentiates the action of CCK to increase both pancreatic-juice flow and amylase release and that raising the glucose concentration in the perfusate potentiates the CCK-induced exocrine secretary response through an increase in endogenous insulin release (Fig. 2 ) . Kanno et al. wrote many articles on the effects of hormones (3-5) and on other factors (2,619) on stimulus-secretion coupling in the exocrine perfused pancreas. Otsuki et al. (19) isolated and perfused rat pancreas according to the technique of Kanno with slight modifications. They measured not only pancreatic-juice flow and amylase output but also insulin (and glucagon) in the portal effluent. Eventually they studied simultaneously both the exocrine and endocrine responses in perfused i...

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“…Previous in vitro studies in rats using natural porcine CCK [2. 13] or cerulein [8,13,14], and in vivo experiments using natural porcine CCK [15] have shown that the insulinotropic effect of CCK is glu cose dependent. This is confirmed in the present study in that even the highest levels of CCK-8 had no effect on insulin release at a perfusate glucose concentration of 2.8 mM ( fig.…”

Section: Discussionmentioning

confidence: 99%

Glucose-Dependent Insulinotropic Action of Cholecystokinin Octapeptide in the Isolated Perfused Rat Pancreas

Müller¹,

Demol²,

Fladrich³

et al. 1983

Digestion

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Whether cholecystokininoctapeptide (CCK-8) stimulates insulin secretion at submaximal or supramaximal levels for pancreatic exocrine secretion was investigated. CCK-8 was delivered to the isolated perfused rat pancreas by a linear gradient ranging from 0 to 1,100 or 0 to 220 pg/ml at two different glucose concentrations. At 2.8 mM glucose CCK-8 was not insulinotropic even at supramaximal stimulation for exocrine pancreatic secretion. At 15.8 mM glucose CCK-8 was insulinotropic starting already at concentrations which were submaximal for stimulation of exocrine pancreatic secretion. It was concluded that CCK-8 warrants consideration as a hormone involved in the enteroinsular axis.

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Glucose-Dependent Insulinotropic Action of Cholecystokinin and Caerulein in the Isolated Perfused Rat Pancreas

Cited by 52 publications

References 23 publications

Pituitary Contents of Beta-Endorphin, Dynorphin, Substance P, Cholecystokinin and Somatostatin in Rats with Streptozotocin-lnduced Diabetes

Pituitary Contents of Beta-Endorphin, Dynorphin, Substance P, Cholecystokinin and Somatostatin in Rats with Streptozotocin-lnduced Diabetes

Exocrine Pancreatic Physiology

Glucose-Dependent Insulinotropic Action of Cholecystokinin Octapeptide in the Isolated Perfused Rat Pancreas

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