Role of antrum in regulation of pancreaticobiliary secretion in humans

Kreiss, Christianna; Schwizer, Werner; Erlacher, U.; Borovicka, Jan; Löchner-Kuery, C.; Müller, Rouven; Jansen, J.B.M.J.; Fried, Michael

doi:10.1152/ajpgi.1996.270.5.g844

Cited by 11 publications

(6 citation statements)

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“…We used a volume of 150 mL water to deliver cholestyramine to the intestine. Apparently, ingestion of even relatively small volumes results in antral distension and can elicit potent cholinergic‐mediated pancreatobiliary secretion 31 . It is theoretically possible that in the present study, early antral distension by the cholestyramine‐containing solution might have initiated motilin release and gallbladder contraction.…”

Section: Discussionmentioning

confidence: 64%

Acute intraduodenal bile salt depletion leads to strong gallbladder contraction, altered antroduodenal motility and high plasma motilin levels in humans

Portincasa

Peeters

Berge-Henegouwen³

et al. 2000

Neurogastroenterology Motil

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Cholecystokinin is the main hormone involved in postprandial gallbladder contraction. There is also considerable gallbladder contraction in the fasting state, associated with phase III of the gastrointestinal migrating motor complex and release of the hormone motilin. It has been proposed that intraduodenal bile salts exert a negative-feedback control on postprandial cholecystokinin release and resulting gallbladder contraction. We wanted to elucidate whether a similar control mechanism on gallbladder contraction exists in the fasting state. We therefore performed gallbladder ultrasonography and 24-h antroduodenal motility registrations and determined plasma cholecystokinin and motilin levels in six healthy subjects before and after acute (4 g) and chronic (8 days; 8 g day(-1)) oral cholestyramine. Acute cholestyramine strongly decreased gallbladder volumes and increased motilin without changed cholecystokinin levels. There was a negative relationship between gallbladder volumes and plasma motilin levels. Although there was a persistent fasting pattern of antroduodenal motility, its cycle length was increased (P < 0.03) with markedly longer phase II (P < 0. 005). Fasting gallbladder volumes 24 h later were still strongly decreased but gradually increased to pretreatment levels. Before and after 8 days cholestyramine, interdigestive and postprandial gallbladder emptying, intestinal migrating motor complex and hormone levels did not differ. We conclude that acute (but not chronic) intraduodenal bile salt depletion with cholestyramine affects gallbladder and antroduodenal motility, possibly partly related to motilin release.

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Section: Discussionmentioning

confidence: 64%

Acute intraduodenal bile salt depletion leads to strong gallbladder contraction, altered antroduodenal motility and high plasma motilin levels in humans

Portincasa

Peeters

Berge-Henegouwen³

et al. 2000

Neurogastroenterology Motil

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“…In particular, the minimal relationship at a genetic level is strongly indicative that the BON cell line is neither EC cell nor intestinal in origin and the secretory and proliferative responses to cholecystokinin and secretory responses to bombesin and acetylcholine further indicate that BON represents a modified pancreatic endocrine cell [73, 74]. The obvious similarities between KRJ-I and the normal EC cells in terms of receptor expression and secretory responses to a variety of neural and luminal stimuli as well as expression of common markers, e.g.…”

Section: Discussionmentioning

confidence: 99%

KRJ-I and BON Cell Lines: Defining an Appropriate Enterochromaffin Cell Neuroendocrine Tumor Model

et al. 2009

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Background: Neuroendocrine tumors (NETs) of the gastrointestinal (GI) system are increasing in incidence with minimal improvement in prognosis. Although the cell of origin has been identified as the enterochromaffin (EC) cell, its secretory and proliferative regulation has not been defined at a mechanistic level. To date, the BON cell line has been the most widely used in vitro EC cell model despite its pancreatic origin. Using whole-genome mathematical analysis as well as secretory and proliferative studies, we compared the BON cell line to the small intestine (SI) EC cell-derived NET cell line, KRJ-I, to assess individual cell line validity and applicability for the investigation of GI-NET disease. Methods and Results: Principal component analysis and ANOVA of KRJ-I and BON transcriptomes (U133 Plus 2) identified substantially different (<10%) overlap in transcripts with minimal (R² = 0.24) correlation in gene expression profiles. RT-PCR detected large variability (>12%) in neuroendocrine (NE) marker transcripts in the BON cell line and the absence of Tph-2, DDC, TGFβR2, and M3 transcripts in KRJ-I. The KRJ-I cell line secreted serotonin (5-HT) in response to isoproterenol (EC₅₀ = 100 nM), noradrenaline (EC₅₀ = 1.7 nM), and pituitary adenylate cyclase (PACAP, EC₅₀ = 0.03 nM). Cholecystokinin (IC₅₀ = 430 nM), somatostatin (IC₅₀ = 400 nM), acetylcholine (IC₅₀ = 3.7 nM), and γ-aminobutyric acid A (GABA_A, IC₅₀ = 2 nM) all inhibited 5-HT release, while gastrin and bombesin had no effect. 5-HT secretion in the BON cell line was stimulated by isoproterenol (EC₅₀ = 900 nM), noradrenaline (EC₅₀ = 20 nM), cholecystokinin (EC₅₀ = 130 nM), PACAP (EC₅₀ = 0.12 nM), bombesin (EC₅₀ = 15 nM), and acetylcholine (EC₅₀ = 0.2 nM). It was inhibited by somatostatin (IC₅₀ = 300 nM) but not GABA_A. KRJ-I responded with proliferation to connective tissue growth factor (CTGF, EC₅₀ = 0.002 ng/ml), transforming growth factor-α (TGFα, EC₅₀ = 0.63 ng/ml) and transforming growth factor-β (TGFβ, EC₅₀ = 0.63 ng/ml). Epidermal growth factor (EGF) and somatostatin had no significant effect. BON cell proliferation was stimulated only by EGF and TGFα (EC₅₀ = 15.8 and 10 ng/ml). TGFβ (IC₅₀ = 0.16 ng/ml), MZ-4-147 (IC₅₀ = 0.5 nM), and BIM23A761 (IC₅₀ = 0.06 nM) all inhibited proliferation. CTGF and somatostatin had no effect. Conclusion: KRJ-I and BON cell lines demonstrate substantial differences in gene level transcripts, inconsistent receptor profile expression, wide variability in NE marker transcript levels, and significantly differential proliferative and secretory responses. Given the EC cell origin of KRJ-I, these results provide evidence that the BON cell line does not represent an EC cell system and is not a valid study model of (carcinoid) EC cell-derived NET.

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“…Therefore, it can be expected that gastrectomy including vagotomy may cause cholelithiasis and bile duct dilatation. [1][2][3][4][5][6] In the past, vagotomy was almost inevitable due to lymph node dissection when performing gastrectomy in patients with gastric cancer, which led to the hypothesis that cholelithiasis is increased after gastrectomy, although the number of reports is limited. [7][8][9] It would be necessary to determine whether the incidence of cholelithiasis has actually increased after surgery, in addition to its complications and clinical characteristics.…”

Section: Introductionmentioning

confidence: 99%

Clinical Significance of Biliary Dilatation and Cholelithiasis after Subtotal Gastrectomy

Yoon

Kwon

Jeong

et al. 2015

Korean J Gastroenterol

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Background/Aims: The well-organized study to support that increased cholelithiasis and bile duct dilatation can occur after gastrectomy has not been reported. The aim of this study was to determine the incidence of cholelithiasis and the degree of common bile duct (CBD) dilatation in patients undergoing subtotal gastrectomy, compared to those undergoing endoscopic treatment for gastric cancer. Methods: Patients who diagnosed with gastric cancer and received treatment at six academic referral centers were investigated for the incidence and time of cholelithiasis and the degree of CBD dilatation after treatment by analysis of 5-year follow-up CTs. The operation group underwent subtotal gastrectomy without vagotomy, while in the control group endoscopic treatment was administered for gastric cancer. Results: A total of 802 patients were enrolled in 5-year analysis (735 patients in the operation group and 67 patients in the control group). Cholelithiasis occurred in 47 patients (6.39%) in the operation group and 3 patients (4.48%) in the control group (p=0.7909). The incidences of cholelithiasis were 4.28% in Billoth-I and 7.89% in Billoth-II (p=0.0487). The diameter of proximal CBD and distal CBD increased by 1.11 mm and 1.41 mm, respectively, in the operation group, compared to 0.4 mm and 0.38 mm, respectively, in the control group (p＜0.05). Patients with increased CBD dilatation more than 5 mm showed statistically significant increases in alkaline phosphatase and gamma-glutamyltransferase. Conclusions: The incidence of cholelithiasis was not increased due to subtotal gastrectomy without vagotomy, but the incidence was higher after Billoth-II compared to Billoth-I. In addition, significant change in the CBD diameter was observed after subtotal gastrectomy. (Korean J Gastroenterol 2015;66:33-40)

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Role of antrum in regulation of pancreaticobiliary secretion in humans

Cited by 11 publications

References 0 publications

Acute intraduodenal bile salt depletion leads to strong gallbladder contraction, altered antroduodenal motility and high plasma motilin levels in humans

Acute intraduodenal bile salt depletion leads to strong gallbladder contraction, altered antroduodenal motility and high plasma motilin levels in humans

KRJ-I and BON Cell Lines: Defining an Appropriate Enterochromaffin Cell Neuroendocrine Tumor Model

Clinical Significance of Biliary Dilatation and Cholelithiasis after Subtotal Gastrectomy

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