Postprandial gallbladder motor function: Refilling and turnover of bile in health and in cholelithiasis

Jazrawi, R. P.; Pazzi, P.; Petroni, Maria Letizia; Prandini, Napoleone; Paul, Catherine; Adam, Jane A.; Gullini, S.; Northfield, T.C.

doi:10.1016/0016-5085(95)90348-8

Cited by 122 publications

(80 citation statements)

References 36 publications

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“…Increased mucin production (among other pronucleating agents) 10,31-33 then leads to the precipitation of cholesterol crystals, which are trapped in the mucin gel 10,25,[31][32][33] and not ejected because of gallbladder stasis. 14,15 Adding erythromycin significantly improved both gallbladder motility and small intestinal transit. This resulted in a more rapid cycling of the bile salt pool, causing higher rates of hepatic bile salt secretion and thus lowering the CSI of both hepatic and gallbladder bile.…”

Section: Discussionmentioning

confidence: 98%

“…3,4,[8][9][10][11][12] Among the growing list of pathogenic events implicated in cholesterol gallstone formation, prolonged intestinal transit and gallbladder stasis both impede enterohepatic cycling and are thus able to lower the bile salt secretion, predisposing to the formation of bile with an increased cholesterol saturation. 10,[13][14][15][16][17] Ground squirrels fed a 1% high-cholesterol diet exhibit abnormal biliary lipid secretion, increased mucin accumulation on the epithelial surface of the gallbladder, defective gallbladder motility, and delayed intestinal transit as the cholesterol saturation in bile increases. [17][18][19] These unique features characterize this well-established animal model and mimic the proposed sequential events in cholesterol gallstone formation in humans.…”

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confidence: 99%

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Effect of the prokinetic agent, erythromycin, in the richardson ground squirrel model of cholesterol gallstone disease

Scott

Tan

et al. 1998

Hepatology

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Section: Discussionmentioning

confidence: 98%

mentioning

confidence: 99%

Effect of the prokinetic agent, erythromycin, in the richardson ground squirrel model of cholesterol gallstone disease

Scott

Tan

et al. 1998

Hepatology

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“…In humans, intestinal cholesterol absorption is known to be appreciably augmented by hypomotility of the small intestine (42). Moreover, gallbladder hypomotility results in prolonged stagnation of bile (43), which is an important risk factor for ChGS, by facilitating phase separation of cholesterol liquid and solid crystals from supersaturated gallbladder bile (3). Most likely, therefore, a key contributing factor to ChGS susceptibility in the Cpe fat mutant mouse is its inability to elevate circulating CCK levels postprandially (37).…”

Section: Discussionmentioning

confidence: 99%

Cholesterol gallstone formation in overweight mice establishes that obesity per se is not linked directly to cholelithiasis risk

Bouchard

Johnson

Carver

et al. 2002

Journal of Lipid Research

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The relationship between obesity and cholesterol cholelithiasis is not well understood at physiologic or genetic levels. To clarify whether obesity per se leads to increased prevalence of cholelithiasis, we examined cholesterol gallstone susceptibility in three polygenic (KK/H1J, NON/LtJ, NOD/LtJ) and five monogenic [carboxypeptidase E ( Cpe fat ), agouti yellow (A y ) , tubby ( tub ), leptin ( Lep ob ), leptin receptor ( Lepr db )] murine models of obesity during ingestion of a lithogenic diet containing dairy fat, cholesterol, and cholic acid. At 8 weeks on the diet, one strain of polygenic obese mice was resistant whereas the others revealed low or intermediate prevalence rates of cholelithiasis. Monogenic obese mice showed distinct patterns with either high or low gallstone prevalence rates depending upon the mutation. Dysfunction of the leptin axis, as evidenced by the Lep ob and the Lepr db mutations, markedly reduced gallstone formation in a genetically susceptible background strain, indicating that in mice with this genetic background, physiologic leptin homeostasis is a requisite for cholesterol cholelithogenesis. In contrast, the Cpe fat mutation enhanced the prevalence of cholelithiasis markedly when compared with the background strain. Since CPE converts many prohormones to hormones, a deficiency of biologically active cholecystokinin is a likely contributor to enhanced susceptibility to cholelithiasis through compromising gallbladder contractility and small intestinal motility. Because some murine models of obesity increased, whereas others decreased cholesterol gallstone susceptibility, we establish that cholesterol cholelithiasis in mice is not simply a secondary consequence of obesity per se. Rather, specific genes and distinct pathophysiological pathways are responsible for the shared susceptibility to both of these common diseases. -Bouchard, G., D. Johnson, T. Carver, B. Paigen, and M. C. Carey. Cholesterol gallstone formation in overweight mice establishes that obesity per se is not linked directly to cholelithiasis risk.

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“…Another outcome was to assess the feasibility of cholescintigraphy in the detection or confirmation of steatocholecystitis. Previous studies indicated that contractility of gallbladder is decreased in patients with fatty gallbladder diseases [14][15][16][17]. The mechanism was postulated as an abnormal fatty deposition in the gallbladder mucosa associated with chronic inflammation and tissue damage, which could result in deterioration of gallbladder function [3,4,7].…”

Section: Discussionmentioning

confidence: 99%

Acute Cholecystitis after Screening Colonoscopy

Jeong¹,

Jung²

2016

Korean J Pancreas Biliary Tract

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Objective. Contractility of gallbladder is known to be decreased in fatty gallbladder diseases. However, clinical estimation data about this relationship is still lacking. The aim of this study was to investigate the association between steatocholecystitis and contractility of gallbladder. Methods. Patients with cholecystitis (steatocholecystitis versus nonsteatocholecystitis) who underwent cholescintigraphy before cholecystectomy were retrospectively evaluated in a single teaching hospital of Korea. The association of steatocholecystitis with contractility of gallbladder, measured by preoperative cholescintigraphy, was assessed by univariable and multivariable analysis. Results. A total of 432 patients were finally enrolled (steatocholecystitis versus nonsteatocholecystitis; 75 versus 357, calculous versus acalculous cholecystitis; 316 versus 116). In the multivariable analysis, age (OR: 0.94, 95% CI: 0.90-0.99, = 0.01) and total serum cholesterol (OR: 1.02, 95% CI: 1.01-1.04, = 0.04) were related to steatocholecystitis in patients with acalculous cholecystitis. Only age (OR: 0.97, 95% CI: 0.94-0.99, = 0.004) was significantly related to steatocholecystitis in patients with calculous cholecystitis. However, ejection fraction of gallbladder reflecting contractility measured by cholescintigraphy was not related to steatocholecystitis irrespective of presence of gallbladder stone in patients with cholecystitis. Conclusion. Ejection fraction of gallbladder measured by cholescintigraphy cannot be used for the detection or confirmation of steatocholecystitis.

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Postprandial gallbladder motor function: Refilling and turnover of bile in health and in cholelithiasis

Cited by 122 publications

References 36 publications

Effect of the prokinetic agent, erythromycin, in the richardson ground squirrel model of cholesterol gallstone disease

Effect of the prokinetic agent, erythromycin, in the richardson ground squirrel model of cholesterol gallstone disease

Cholesterol gallstone formation in overweight mice establishes that obesity per se is not linked directly to cholelithiasis risk

Acute Cholecystitis after Screening Colonoscopy

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