The second finding of the present study was the evidence, albeit indirect, that the gallbladder mucosa absorbs significant amounts of both cholesterol and phospholipids during fasting. This process was much more efficient in many gallstone-free controls than in either gallstone patients or morbidly obese gall-stone-free subjects. When the samples with cholesterol super-saturation are separately considered for correlation analysis, both the cholesterol and phospholipid concentrations increase linearly in relation to the bile salt concentration in all the disease study groups, indicating that about 25% of both cholesterol and phospholipids had been absorbed from bile during fasting. The linear relationships that emerged between lipid concentrations in gallbladder bile confirms previous data on gallbladder bile and on hepatic bile obtained in T-tube patients. However, most of published data on hepatic secretion obtained by duodenal sampling under continuous gallbladder contraction have shown by perbolic lipid relationships. The most likely explanation for this apparent discrepancy is that when the enterohepatic circulation is interrupted, as after bile diversion, or decreased, as during an overnight fasting, the bile salt output is diminished to a range where the secretion of both cholesterol and phospholipids is linearly related to that of bile salts.

Our data showing no lipid correlation in the supersaturated samples obtained from nonobese gallstone-tree controls can be explained by the fact that half the samples in this group had much lower relative (%) concentrations of both cholesterol and phospholipids. Our interpretation is that in about half of the gall stone-free control subjects a highly efficient but variable mucosal absorption of cholesterol and phospholipids occurs.

When the cholesterol-undersaturated samples are analyzed in comparable lipid plots, the phospholipid but nọt the cholesterol pattern resembles that found in the supersaturated samples. In undersaturated samples, cholesterol and bile salt concentrations positively correlated in all groups including controls but showed no evidence for cholesterol absorption. Both this unexpected finding in undersaturated samples of all groups, as well as the results in the supersaturated samples of the control group showing a highly variable lipid absorption could be explained if the composition of the bile entering the gallbladder lumen were a major determinant of cholesterol absorption. In keeping with this hypothesis, it has previously been shown in vitro that cholesterol absorption by the gallbladder increases with increasing cholesterol concentration and saturation of bile.

Our data are amenable to more than one interpretation. We believe it is most likely that our lipid plots express a less efficient gallbladder mucosal lipid absorption process in the four disease study groups compared to controls and thạt this malfunction is concomitant with the fluid absorption defect. However. it cannot be excluded that our lipid plots are, other than an expression of gallbladder lipid absorption. at least partially influenced by difterences in hepatic bile composition between controls and all the disease study groups. It would have been useful to compare lipid plots in hepatic and gallbladder bile in all groups of our study, including controls. However, as common duct bile sampling is unethical in gallstone free subjects, the comparison would have been possible only in gallstone patients, who represent only a minor part of our study population. Nevertheless, in our opinion, the role played by gallbladder lipid absorption is of major importance for the following reason: we have recently directly measured, in vitro. lipid absorption from a supersaturated bile by the intact human gallbladder. Within 5 hr. 23% of biliary cholesterol and 30% of phosphatidylcholine was absorbed by the gallbladder in the absence of cholesterol gallstone disease. Moreover the rate of lipid absorption was found to be significantly reduced (about halt) in gallbladder with cholesterol gallstone disease. These values, obtained within 5 hr, i.e., approximately half the time span of nocturnal fasting, are in keeping with the conclusions of the present paper.

To conclude, the findings of this study clearly document that fasting gallbladder bile samples from nonobese stone-free control subjects are consistently more concentrated than those of cholesterol gallstone patients and morbidly obese subjects with or without gallstones. Indirect evidence of gallbladder mucosal absorption of appreciable amounts of cholesterol and phospholipid was also found, this process being more pronounced in controls than in the disease study groups. Impaired gallbladder mucosal function is not necessarily a consequence of gallstone disease.

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