The potential site of impaired gallbladder contractility in an animal model of cholesterol gallstone disease

Chen, Nansheng; Shaffer, E.A.

doi:10.1053/gast.1996.v110.pm8536864

Cited by 45 publications

(55 citation statements)

References 2 publications

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“…It has been described that aging compromises gallbladder function and drives to an elevated incidence of cholesterol gallstones in old individuals (Chen et al 1999;van de Heijning et al 1999;Xu and Shaffer 1996). We found that aging modifies neurological control of guinea pig gallbladder and impairs contractile response as the result of alterations in the contractile machinery without affecting calcium release from intracellular stores (Gomez-Pinilla et al 2006).…”

Section: Introductionmentioning

confidence: 51%

Aging impairs Ca2+ sensitization pathways in gallbladder smooth muscle

Macias

Gomez‐Pinilla

Camello-Almaraz

et al. 2011

AGE

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Calcium sensitization is an important physiological process in agonist-induced contraction of smooth muscle. In brief, calcium sensitization is a pathway that leads to smooth muscle contraction independently of changes in [Ca 2+ ] i by mean of inhibition of myosin light chain phosphatase. Aging has negative impacts on gallbladder contractile response due to partial impairment in calcium signaling and alterations in the contractile machinery. However, information regarding aging-induced alterations in calcium sensitization is scanty. We hypothesized that the calcium sensitization system is negatively affected by age. To investigate this, gallbladders were collected from adult (4 months old) and aged (22-24 months old) guinea pigs. To evaluate the contribution of calcium sensitization pathways we assayed the effect of the specific inhibitors Y-27632 and GF109203X on the "in vitro" isometric gallbladder contractions induced by agonist challenges. In addition, expression and phosphorylation (as activation index) of proteins participating in the calcium sensitization pathways were quantified by Western blotting. Aging reduced bethanechol-and cholecystokinin-evoked contractions, an effect associated with a reduction in MLC20 phosphorylation and in the effects of both Y-27632 and GF109203X. In addition, there was a drop in ROCK I, ROCK II, MYPT-1 and PKC expression and in the activation/phosphorylation of MYPT-1, PKC and CPI-17 in response to agonists. Interestingly, melatonin treatment for 4 weeks restored gallbladder contractile responses due to re-establishment of calcium sensitization pathways. These results demonstrate that agerelated gallbladder hypocontractility is associated to alterations of calcium sensitization pathways and that melatonin treatment exerts beneficial effects in the recovery of gallbladder contractility.

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Section: Introductionmentioning

confidence: 51%

Aging impairs Ca2+ sensitization pathways in gallbladder smooth muscle

Macias

Gomez‐Pinilla

Camello-Almaraz

et al. 2011

AGE

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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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“…This often, but not always, reduces gallbladder motility because of exces sive accumulation of cholesterol esters within epithelial macrophages of the gallbladder wall and formation of foam cells (cholesterolosis). Gallbladder dysfunction is caused by cholesterol action on sarcoleme membrane of the gallbladder smooth muscles [13]. However, some patients with cholesterolosis have a normal functioning gallbladder, as in the case of patient P. Cholesterol in bile is accumulated as micelles and vesicles under normal physiologic conditions.…”

Section: Discussionmentioning

confidence: 99%

Gallstone Disease and Cholesterolosis in Monozygotic Twin Sisters

Ivanchenkova

Шарашкина

Martirosyan

et al. 2007

Balkan Journal of Medical Genetics

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Gallstone disease and cholesterolosis may be inde pendent diseases or forms of the same disease, caused by impairment of cholesterol metabolism. Gallstone disease is characterized by formation of cholesterol concrements in the gallbladder cavity. Cholesterolosis is a hyperplastic cholecistosis, caused by cholesterol accumulation in the gallbladder wall with subsequent proliferation of gallblad der normal tissue elements. We describe monozygotic twin sisters, one of whom developed gallstone disease and the other developed cholesterolosis. Monozygosity was veri fied by a DNA fingerprinting method. Both had identical heterogeneity of plasma low density lipoprotein (LDL) subfractions, but associated with different functional con ditions within the gallbladder. The different manifestations may be due to epigenetic, metabolic or environmental factors, since both had a common genetic basis.

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The potential site of impaired gallbladder contractility in an animal model of cholesterol gallstone disease

Cited by 45 publications

References 2 publications

Aging impairs Ca2+ sensitization pathways in gallbladder smooth muscle

Aging impairs Ca2+ sensitization pathways in gallbladder smooth muscle

Acute Cholecystitis after Screening Colonoscopy

Gallstone Disease and Cholesterolosis in Monozygotic Twin Sisters

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