Published online Jul 28, 2014. doi: 10.3748/wjg.v20.i28.9513
Revised: March 19, 2014
Accepted: April 21, 2014
Published online: July 28, 2014
Processing time: 195 Days and 11.1 Hours
AIM: To investigate the role of caveolin-3 (CAV3) and cholecystokinin A receptor (CCKAR) in cholesterol gallstone disease (CGD).
METHODS: To establish a mouse model of CGD, male C57BL/6 mice were fed with a lithogenic diet containing 1.0% cholic acid, 1.25% cholesterol and 15% fat; a similar control group was given a normal diet. The fresh liver weights and liver-to-body weight ratio were compared between the two groups after one month. Serum lipid profile and bile composition were determined with an autoanalyzer. The Cav3 and Cckar mRNA and CAV3 and CCKAR protein levels in the liver and gallbladder were determined via real-time polymerase chain reaction and Western blot, respectively.
RESULTS: Establishment of the mouse CGD model was verified by the presence of cholesterol gallstones in mice fed the lithogenic diet. Compared with mice maintained on a normal diet, those fed the lithogenic diet had significantly higher mean liver-to-body weight ratio (0.067 ± 0.007 vs 0.039 ± 0.007, P < 0.01), serum total cholesterol (4.22 ± 0.46 mmol/L vs 2.21 ± 0.11 mmol/L, P < 0.001), bile total cholesterol (1.33 ± 0.33 mmol/L vs 0.21 ± 0.11 mmol/L, P < 0.001), and bile phospholipid concentrations (3.55 ± 1.40 mmol/L vs 1.55 ± 0.63 mmol/L, P = 0.04), but lower total bile acid concentrations (726.48 ± 51.83 μmol/L vs 839.83 ± 23.74 μmol/L, P = 0.007). The lithogenic diet was also associated with significantly lower CAV3 in the liver and lower CAV3 and CCKAR in the gallbladder compared with the control mice (all P < 0.05).
CONCLUSION: CAV3 and CCKAR may be involved in cholesterol gallstone disease.
Core tip: Cholesterol gallstone disease (CGD) is one of the most common digestive diseases worldwide, while the mechanisms of this disease are not fully understood. In this study, we established a mouse model of CGD and observed that the formation of gallstones was accompanied by an increase in serum and bile total cholesterol concentrations, while by a decrease in total bile acid concentration in bile. The formation of gallstones was also accompanied by downregulation of hepatic caveolin-3 (CAV3) expression, and downregulation of CAV3 and cholecystokinin A receptor (CCKAR) expression in the gallbladder. Our results suggest that CAV3 and CCKAR may be involved in CGD.