Cephalic Stimulation of Gallbladder Contraction in Humans: Role of Cholecystokinin and the Cholinergic System

Hopman, W. P. M.; Jansen, J. B. M. J.; Rosenbusch, Gerd

doi:10.1159/000199592

Cited by 77 publications

(31 citation statements)

References 16 publications

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“…CCK is not involved in the regulation of the cephalic pancreatic response, since plasma CCK levels did not significantly increase during sham feeding, and CCK receptor blockade with loxiglumide does not affect the magnitude of the cephalic stimulated pancreatic exocrine response [15]. The observation that sham feeding increases the duodenal bilirubin output is in agreement with studies showing gallbladder contraction of up to 40% after cephalic stimulation [5, 24]. Increases in duodenal bilirubin output are highly correlated with reductions in gallbladder volume measured by ultrasonography [25].…”

Section: Discussionsupporting

confidence: 77%

Hyperglycemia Reduces Pancreaticobiliary Secretion in Response to Modified Sham Feeding in Humans

Lam¹,

Lindeboom²,

Lamers³

et al. 1999

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Background/Aims: We have investigated the effect of acute hyperglycemia on pancreaticobiliary secretion and pancreatic polypeptide (PP) release. Methods: Duodenal outputs of bilirubin, trypsin, lipase, amylase and bicarbonate were measured using a recovery marker under basal conditions and in response to modified sham feeding (MSF) in 6 healthy subjects on two separate occasions: during normoglycemia and during acute hyperglycemia (15 mmol/l). Results: During hyperglycemia the basal pancreaticobiliary output was significantly (p < 0.05) reduced. During normoglycemia MSF significantly (p < 0.05) increased the output of bilirubin and pancreatic enzymes; during hyperglycemia only the output of pancreatic enzymes increased significantly (p < 0.05) over basal. During MSF the outputs of bilirubin (16 ± 4 vs. 4 ± 2 µmol/30 min), trypsin (26 ± 7 vs. 7 ± 4 U/30 min), lipase (36 ± 11 vs. 15 ± 6 kU/30 min), amylase (3.4 ± 0.7 vs. 1.4 ± 0.7 kU/30 min) and bicarbonate (0.8 ± 0.1 vs. 0.5 ± 0.1 mmol/30 min) were significantly (p < 0.05) reduced during hyperglycemia compared to normoglycemia. During hyperglycemia basal and MSF-stimulated PP levels were significantly (p < 0.05) reduced compared to normoglycemia. MSF did not significantly influence plasma cholecystokinin levels in both experiments. Conclusions: This study indicates (1) that the blood glucose levels affect basal and cephalic stimulated pancreaticobiliary secretion and (2) that the PP secretion during hyperglycemia is reduced, suggesting impaired vagal cholinergic activity during hyperglycemia.

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Section: Discussionsupporting

confidence: 77%

Hyperglycemia Reduces Pancreaticobiliary Secretion in Response to Modified Sham Feeding in Humans

Lam¹,

Lindeboom²,

Lamers³

et al. 1999

Digestion

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“…Serum glucose concentrations were measured every 2.5 to 5 rnin according to the glucose oxidase method (Beckman glucose analyzer; Beckman Instruments, Palo Alto, CAI. Gallbladder images were obtained in duplicate every 15 rnin under basal conditions for 60 min (-60 to 0 min), after stimulation with modified sham feeding (MSF) for 90 min (0 to 90 min) and after regular feeding of the same meal used for MSF for 60 rnin (90 to 150 rnin). During the first 30 min after the start of MSF and regular feeding, gallbladder images were taken every 10 min.…”

Section: Methodsmentioning

confidence: 99%

Hyperglycemia reduces gallbladder emptying and plasma hormone secretion to modified sham feeding and regular feeding

et al. 1993

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The purpose of this study was to investigate the effect of acute stable hyperglycemia on gallbladder motility, plasma cholecystokinin level and pancreatic polypeptide secretion. Gallbladder emptying in response to modified sham feeding and regular feeding was determined in six healthy subjects on two separate occasions during normoglycemia (serum glucose = 5 mmol/L) and during hyperglycemia (serum glucose = 15 mmol/L). Pancreatic polypeptide secretion was determined as an indirect measure of cholinergic tone. Gallbladder contraction in response to sham feeding during hyperglycemia (9% f 2%) was significantly (p < 0.05) reduced compared with that in normoglycemia (22% & 1%). During hyperglycemia, gallbladder emptying after meal ingestion (29% f 9%) was significantly (p < 0.05) less than that in normoglycemia (60% & 10%). Sham feeding did not affect plasma cholecystokinin levels. Regular feeding induced significant (p < 0.05) increases in plasma cholecystokinin levels in both experiments. However, integrated postprandial plasma cholecystokinin secretion was significantly (p < 0.05) reduced during hyperglycemia compared with that in normoglycemia (29 f 5 pmol e 60 min vs. 58 f 10 pmol-60 min). Modified sham feeding-and feeding-stimulated pancreatic polypeptide secretion during hyperglycemia (235 f 95 pmol a 90 rnin and 1,035 f 267 pmol * 60 min, respectively) were significantly (p < 0.05) less than levels seen in normoglycemia (434 f 71 pmol .90 rnin and 1,961 f 219 pmol * 60 min, respectively). This study indicates that gallbladder emptying and plasma hormone secretion in response to sham feeding and regular feeding are affected by blood glucose levels. ( duced by intravenous infusion of glucose decreases the rate of gastric emptying of solid and liquid meals (1, 4). In patients with diabetes mellitus, disorders of gastrointestinal motility and secretion occur frequently (5). Abnormal gastrointestinal function in these patients has been associated with the presence of autonomic neuropathy (5, 6). Apart from vagal nerve dysfunction, however, other factors such as glycemic control may be involved. Indeed, in recent studies a relationship between hyperglycemia and delayed gastric emptying has been demonstrated in patients with type I and I1 diabetes mellitus (7, 8). Little is known, however, about the role of serum glucose in the regulation of gallbladder motor function (9). This study was undertaken to investigate the influence of hyperglycemia on gallbladder contraction induced by sham feeding and regular feeding. Gallbladder motility and endogenous cholecystokinin (CCK) secretion, as the major hormonal stimulus for gallbladder contraction, were determined during normoglycemia (serum glucose concentration = 5 mmol/L) and hyperglycemia (serum glucose concentration = 15 mmol/L). A second goal of the study was to examine the tone of the cholinergic system during hyperglycemia. This was accomplished indirectly by measuring pancreatic polypeptide (PP) secretion, which is known to be dependent on cholinergic tone.

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“…MSF was performed using the 'chew and spit' technique involv ing chewing and careful expectoration of small portions of a meal for 30 min [12,13], The subjects were instructed not to swallow a single morsel of food. Gastric aspirates were carefully checked for swal lowed food particles, and none were found.…”

Section: Test Proceduresmentioning

confidence: 99%

Hyperglycemia Reduces Gastric Secretory and Plasma Pancreatic Polypeptide Responses to Modified Sham Feeding in Humans

et al. 1993

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We have investigated the effect of acute stable hyperglycemia on gastric acid secretion and serum gastrin and pancreatic polypeptide (PP) release. Gastric acid output was measured under basal conditions and in response to modified sham feeding (MSF) in 7 healthy volunteers on two separate occasions: during normoglycemia (serum glucose 5 mmol/l) and during hyperglycemia (serum glucose 15 mmol/l). PP secretion was determined as an indirect measure of vagal-cholinergic tone. Basal acid output during hyperglycemia (4.7 ± 1.0 mmol/h) was not significantly different from euglycemia (5.4 ± 0.6 mmol/h), but MSF-stimulated acid output during hyperglycemia (14.7 ± 3.3 mmol/90 min) was significantly (p < 0.05) reduced compared to euglycemia (24.7 ± 3.2 mmol/90 min). Serum gastrin levels were not affected by MSF. During hyperglycemia, the integrated PP secretion in response to MSF (235 ± 95 pmol/l · 90 min) was significantly (p < 0.05) reduced compared to euglycemia (434 ± 71 pmol/l · 90 min). This study indicates that (1) serum glucose affects cephalic-stimulated gastric acid secretion, and (2) PP secretion after MSF is significantly reduced during hyperglycemia suggesting impaired vagal-cholinergic activity during hyperglycemia.

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Cephalic Stimulation of Gallbladder Contraction in Humans: Role of Cholecystokinin and the Cholinergic System

Cited by 77 publications

References 16 publications

Hyperglycemia Reduces Pancreaticobiliary Secretion in Response to Modified Sham Feeding in Humans

Hyperglycemia Reduces Pancreaticobiliary Secretion in Response to Modified Sham Feeding in Humans

Hyperglycemia reduces gallbladder emptying and plasma hormone secretion to modified sham feeding and regular feeding

Hyperglycemia Reduces Gastric Secretory and Plasma Pancreatic Polypeptide Responses to Modified Sham Feeding in Humans

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