Cholecystokinin, Secretin, Pancreatic Polypeptide in Relation to Gallbladder Dynamics and Gastrointestinal Interdigestive Motility

Qvist, Niels; Oster-Jørgensen, E; Rasmussen, Lars Melholt; Pedersen, Sidsel Arnspang; Olsen, Ole; Cantor, Per; Muckadell, Ove B. Schaffalitzky de

doi:10.1159/000200234

Cited by 14 publications

(7 citation statements)

References 30 publications

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“…Secretion of pancreatic polypeptide from the pancreas is known to be under vagal‐cholinergic control 27 . The present study confirms that plasma pancreatic polypeptide levels fluctuate cyclically with the phases of the MMC 28 . Plasma pancreatic polypeptide levels were relatively low during phase I and early phase II, but increased significantly during late phase II and peaked during phase III.…”

Section: Discussionsupporting

confidence: 88%

“…27 The present study con®rms that plasma pancreatic polypeptide levels¯uctuate cyclically with the phases of the MMC. 28 Plasma pancreatic polypeptide levels were relatively low during phase I and early phase II, but increased signi®cantly during late phase II and peaked during phase III. These data support the hypothesis that the cholinergic system is involved in regulating the interdigestive`housekeeper', as recently suggested.…”

Section: Discussionmentioning

confidence: 94%

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Interdigestive antroduodenal motility and gastric acid secretion

Gielkens

Nieuwenhuizen

Biemond

et al. 1998

Aliment Pharmacol Ther

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 94%

Interdigestive antroduodenal motility and gastric acid secretion

Gielkens

Nieuwenhuizen

Biemond

et al. 1998

Aliment Pharmacol Ther

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“…Secretion of PP from the pancreas is known to be under vagal cholinergic control [28] and varies cyclically with the different phases of the MMC [29]. In the present study, plasma PP fluctuations were significantly reduced during both hyperglycaemic and euglycaemic hyperinsulinaemia with little or no increase during late phase II or phase III.…”

Section: Discussionsupporting

confidence: 51%

Is the effect of acute hyperglycaemia on interdigestive antroduodenal motility and small‐bowel transit mediated by insulin?

Gielkens¹,

Verkijk²,

Frölich

et al. 1997

Eur J Clin Investigation

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Acute hyperglycaemia inhibits antroduodenal motility. In non-diabetic subjects this inhibitory effect may result from reactive endogenous hyperinsulinaemia. Therefore, we investigated the effects of hyperinsulinaemia during both hyperglycaemia and euglycaemia on interdigestive antroduodenal motility (perfusion manometry) and duodenocaecal transit time (DCTT; lactulose breath-H2 test). Six healthy volunteers (age 20-26 years) were studied for 240 min on three separate occasions in random order during: (a) i.v. saline (control); (b) acute hyperglycaemic hyperinsulinaemia (HG) with plasma glucose at 15 mmolL-1; and (c) euglycaemic hyperinsulinaemia (HI) with plasma insulin at 80 mUL-1 and glucose at 4-5 mmolL-1, RESULTS: DCTT was significantly (P < 0.05) prolonged during HG (158 +/- 23 min) compared with control (95 +/- 25 min), whereas HI had no effect (100 +/- 17 min). Mean duration of complete migrating motor complex (MMC) cycles was significantly (P < 0.05) reduced during HG (63 +/- 9 min) compared with control (103 +/- 15 min) and HI (105 +/- 16 min), which resulted from a significantly (P < 0.05) shorter duration of phase II. Antral motility was significantly (P < 0.05) reduced during both HI (20 +/- 8 contractions 240 min-1) and HG (9 +/- 5) compared with control (43 +/- 7). It is concluded that in healthy subjects hyperglycaemia prolongs DCTT, increases duodenal MMC cycle frequency and inhibits antral motility. Hyperinsulinaemia reduces antral motor activity but has no effect on interdigestive duodenal motility or DCTT. Thus, other factors, apart from insulin, mediate the inhibitory effect of hyperglycaemia on interdigestive intestinal motility and transit.

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“…Whether it directly affects the acinar cell or indirectly modulates pancreatic secretion through peripheral or central neural pathways, through the release of regulatory peptides, or through changes in splanchnic blood flow, remains to be elucidated. Blockade of CCK-A receptors by loxiglumide did not interrupt the cyclic interdigestive pattern (79), nor do CCK plasma levels fluctuate with the interdigestive phases (80). Loxiglumide did, however, prolong phase I with a compensatory shortening of phase I1 (79).…”

Section: Other Control Mechanismsmentioning

confidence: 99%

Neurohormonal Control of Human Pancreatic Exocrine Secretion

et al. 1995

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Near the end of the last century, Pavlov suggested that pancreatic secretion was exclusively controlled by neural reflex mechanisms (1). In 1902, Bayliss and Starling published their results on secretin, opening the field of gastrointestinal endocrinology while arguing that neural regulation of the pancreas is "superfluous and improbable" (2). In the following decades, especially after the discovery of cholecystokinin (CCK), it was generally held that exocrine pancreatic secretion is mainly regulated by hormones. Thus, investigators have historically tended to adopt an "all-or-nothing" approach; current appreciation of the complexity of mechanisms governing most biologic phenomena leads us to accept that the pancreas is regulated through an interplay of multiple neural and hormonal pathways.Several factors have impeded conclusive definition of the relative contribution of neural and hormonal control of pancreatic secretion. First, the information accumulated over the last several years clearly indicates that results obtained in one species cannot be directly transferred to another. Second, many conclusions were based on infusion of regulatory peptides at supraphysiologic concentrations, which may not accurately reveal their physiologic role. Sensitive and specific assays detecting postprandial plasma levels have now been established for most relevant substances. Third, even infusion of peptides at postprandial plasma levels may not fully elucidate their role as physiologic mediators.Plasma levels obtained from peripheral veins do not necessarily reflect concentrations at the pancreatic receptor, and exogenous infusion may not accurately mimic endogenous release. Fourth, selective receptor antagonists for the peptides in question have only recently become available. The application of effective receptor blockers (e.g., pentanoic acid and benzodiazepine derivatives for CCK receptors) has greatly aided our understanding of physiologic roles. Fifth, pancreatic function is regulated not only by peptide hormones from gastrointestinal endocrine cells, but also by regulatory peptides localized in pancreatic nerve fibers. Finally, pancreatic function is integrated through a complex interaction of mucosal, humoral, neural, and myogenic factors that regulate gastrointestinal secretion and motility. Analysis of a single factor allows only a limited view of pancreatic function as an integral component of the gastroenteropancreatic system.In this review, we have attempted to bring together findings from our groups and others, in order to provide an integrative concept of the neurohormonal systems controlling human exocrine pancreatic secretion. This overview evolved from the first Frank Pickering Brooks Basic Science Lecture, given by the first author at the American Pancreatic Association in 1992. For further review of the regulation of pancreatic exocrine secretion in man and other species, we also refer the reader to several excellent reviews published recently (3-7). EFFECTS OF EXOGENOUS ADMINISTRATION OF SECRETAGOGUESIntr...

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Cholecystokinin, Secretin, Pancreatic Polypeptide in Relation to Gallbladder Dynamics and Gastrointestinal Interdigestive Motility

Cited by 14 publications

References 30 publications

Interdigestive antroduodenal motility and gastric acid secretion

Interdigestive antroduodenal motility and gastric acid secretion

Is the effect of acute hyperglycaemia on interdigestive antroduodenal motility and small‐bowel transit mediated by insulin?

Neurohormonal Control of Human Pancreatic Exocrine Secretion

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