Gallbladder dysfunction enhances physical density but not biochemical metastability of biliary vesicles

The gallbladder role in cholesterol gallstone pathogenesis occurs through m odulation of bile cholesterol metastability. The present study characterize d the effects of concentrating bile on cholesterol crystallization through vesicle transformation, crystal habits, and potentiation of effector substa nces. Supersaturated model biles with total lipid concentrations of 12, 9, 6, and 3 g/dl were prepared with identical molar ratios (taurocholate-egg y olk phosphatidylcholine-cholesterol: 71:18:11). Bile metastability was asse ssed spectrophotometrically, and morphology of vesicle and crystal was sequ entially scanned by video-enhanced differential contrast microscopy. The ef fects of replacing 30% of egg yolk phosphatidylcholine with soy bean phosph atidylcholine, 30% of taurocholate with taurodeoxycholate or tauroursodeoxy cholate, and addition of concanavalin A-binding glycoprotein on each model bile were examined. By lowering total lipid concentration, cholesterol crys tallization was retarded with less fusion and aggregation of vesicles. The effects of substances promoting cholesterol crystallization were enhanced w ith lesser bile. By replacing 30% of taurocholate with tauroursodeoxycholat e, cholesterol crystallization was markedly inhibited in all concentrations , forming stable liquid-crystals. Impaired water absorption by the gallblad der may stabilize vesicles and inhibit rapid cholesterol crystallization, b ut the potential of cholesterol crystallization effector substances must be modified to alter bile cholesterol metastability.