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

Abstract

The gallbladder role in cholesterol gallstone pathogenesis occurs through modulation of bile cholesterol metastability. The present study characterized the effects of concentrating bile on cholesterol crystallization through vesicle transformation, crystal habits, and potentiation of effector substances. Supersaturated model biles with total lipid concentrations of 12, 9, 6, and 3 g/dl were prepared with identical molar ratios (taurocholate-egg yolk phosphatidylcholine-cholesterol: 71:18:11). Bile metastability was assessed spectrophotometrically, and morphology of vesicle and crystal was sequentially scanned by video-enhanced differential contrast microscopy. The effects of replacing 30% of egg yolk phosphatidylcholine with soy bean phosphatidylcholine, 30% of taurocholate with taurodeoxycholate or tauroursodeoxycholate, and addition of concanavalin A-binding glycoprotein on each model bile were examined. By lowering total lipid concentration, cholesterol crystallization was retarded with less fusion and aggregation of vesicles. The effects of substances promoting cholesterol crystallization were enhanced with lesser bile. By replacing 30% of taurocholate with tauroursodeoxycholate, cholesterol crystallization was markedly inhibited in all concentrations, forming stable liquid-crystals. Impaired water absorption by the gallbladder may stabilize vesicles and inhibit rapid cholesterol crystallization, but the potential of cholesterol crystallization effector substances must be modified to alter bile cholesterol metastability.