Literature DB >> 15786550

Gallbladder motor function, plasma cholecystokinin and cholecystokinin receptor of gallbladder in cholesterol stone patients.

Jian Zhu1, Tian-Quan Han, Sheng Chen, Yu Jiang, Sheng-Dao Zhang.   

Abstract

AIM: To study the interactive relationship of gallbladder motor function, plasma cholecystokinin (CCK) and cholecystokinin A receptor (CCK-R) of gallbladder in patients with cholesterol stone disease.
METHODS: Gallbladder motility was studied by ultrasonography in 33 patients with gallbladder stone and 10 health subjects as controls. Plasma CCK concentration was measured by radioimmunoassay in fasting status (CCK-f) and in 30 min after lipid test meal (CCK-30). Radioligand method was employed to analyze the amount and activity of CCK-R from 33 gallstone patients having cholecystectomy and 8 persons without gallstone died of severe trauma as controls.
RESULTS: The percentage of cholesterol in the gallstone composition was more than 70%. The cholesterol stone type was indicated for the patients with gallbladder stone in this study. Based on the criterion of gallbladder residual fraction of the control group, 33 gallstone patients were divided into two subgroups, contractor group (14 cases) and non-contractor group (19 cases). The concentration of CCK-30 was significantly higher in non-contractor group than that in both contractor group and control group (55.86+/-3.86 pmol/L vs 37.85+/-0.88 pmol/L and 37.95+/-0.74 pmol/L, P<0.01), but there was no difference between contractor group and control group. Meanwhile no significant difference of the concentration of CCK-f could be observed among three groups. The amount of CCK-R was lower in non-contractor group than those in both control group and contractor group (10.27+/-0.94 fmol/mg vs 24.59+/-2.39 fmol/mg and 22.66+/-0.55 fmol/mg, P<0.01). The activity of CCK-R shown as KD in non-contractor group decreased compared to that in control group and contractor group. Only was the activity of CCK-R lower in contractor group than that in control group. The ejection fraction correlated closely with the amount of CCK-R (r = 0.9683, P<0.01), and the concentration of CCK-30 correlated negatively with the amount of CCK-R closely (r = -0.9627, P<0.01).
CONCLUSION: The distinctive interactive relationship of gallbladder emptying, plasma CCK and CCK-R in gallbladder from this study suggested that the defect of CCK-R may be a key point leading to the impairment of gallbladder motor function and the pathogenesis of cholesterol gallstone formation may differ in two subgroups of gallstone patient, gallbladder non-contractor group or contractor group.

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Year:  2005        PMID: 15786550      PMCID: PMC4305954          DOI: 10.3748/wjg.v11.i11.1685

Source DB:  PubMed          Journal:  World J Gastroenterol        ISSN: 1007-9327            Impact factor:   5.742


  22 in total

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6.  Excess membrane cholesterol alters human gallbladder muscle contractility and membrane fluidity.

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7.  Correlation of cholecystokinin receptors with gallbladder contractility in patients with gallstones.

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Review 9.  Gallbladder motility, gallstones, and the surgeon.

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10.  Inositol trisphosphate restores impaired human gallbladder motility associated with cholesterol stones.

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  15 in total

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3.  Pathophysiological significance of gallbladder volume changes in gallstone diseases.

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4.  Decreased expression of stem cell factor mRNA and protein in the gallbladders of guinea pigs fed on high cholesterol diet.

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5.  Disruption of the murine protein kinase Cbeta gene promotes gallstone formation and alters biliary lipid and hepatic cholesterol metabolism.

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6.  A genomewide search finds major susceptibility loci for gallbladder disease on chromosome 1 in Mexican Americans.

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7.  Endogenous elevation of plasma cholecystokinin does not prevent gallstones.

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9.  Prevention of gallbladder hypomotility via FATP2 inhibition protects from lithogenic diet-induced cholelithiasis.

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Review 10.  Role of CCK/gastrin receptors in gastrointestinal/metabolic diseases and results of human studies using gastrin/CCK receptor agonists/antagonists in these diseases.

Authors:  Marc J Berna; Robert T Jensen
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