Gallbladder mucosal absorption of fluid during fasting is a well-known process. Indirect in vivo and recent in vitro evidence for physiologically relevant gallbladder absorption of cholesterol and phospholipids from bile has been observed in humans. The present study explored and compared by indirect means the relative efficiencies of human gallbladder mucosal absorption of fluid and lipids in health and disease. Biliary lipids and pigment content were measured in fasting gallbladder bile samples obtained from gallstone-free controls and from four study groups: multiple and solitary cholesterol gallstone patients, and morbidly obese subjects with and without gallstones.

Bile salts and pigment content were significantly greater in gall stone-free controls thạn in all other disease study groups. This was interpreted as evidence of more effective gallbladder mucosal fluid absorption in nonobese gallstone-free controls compared to that in all other groups. Correlation plot analysis of biliary lipids showed tower concentrations of phospholipids than expected from the index bile salt concentrations. The same was found for cholesterol concentrations but only in supersaturated samples. These findings were much more pronounced in gall stone-free controls and were accordingly interpreted as evidence of more efficient gallbladder absorption of both phospholipids and cholesterol in controls compared with that found in each of the disease study groups. Moreover, impaired gallbladder mucosal function, while invariably associated with cholesterol gallstone disease, was not found to be a necessary consequence of the physical presence of stones. lt is concluded that efficient gallbladder mucosal absorption of both fluid and apolar lipids from bile is a normal physiological process that is often seriously impaired in the presence of either cholesterol gallstone disease or at least one of its precursor forms.

Our data show that fluid absorption by the gallbladder is impaired in the presence of gallstone disease. The defect is also observed despite the absence of gallstones when morbid obesity, a known risk factor for gallstones, is present. Fluid absorption by the gallbladder is very difficult to quantitate in vivo prospectively in humans. In the present study we indirectly derived information on the efficiency of fluid absorption in different settings by measuring the concentrations of nonabsorbable bile solutes, i.е. , biliary pigments and bile salts, in a single sample of gallbladder bile obtained from a large number of subjects. We found that, after overnight fasting, non.obese stone-free control subjects have both a significantly higher gallbladder bile salt concentration and pigment content than all the other study groups. Our explanation for these differences is that gallbladders in the control group absorb fluid more efficiently thạn those of the other study groups.

It is highly unlikely that the striking differences we found in nonabsorbable biliary solute (i. e. , conjugated bile salt and pigments) concentrations in gallbladder bile between the non-obesestone-free control and the other four study groups can be explained by differences in their intraluminal accumulation rather than in fluid absorption. There are several reasons for this. First, although bile salt and bilirubin secretion rates of hepatic bite are known to be independent, our results show a similar pattern of variations for both bile salts and total pigments for each of the study groups. Second, the bile salt concentration in common duct bile sampled after overnight fasting of subjects free of gallstone disease is significantly lower than in cholesterol gallstone patients, while in gallbladder bile an opposite trend is observed. Third, even if decreased rates of bile salt hepatic secretion in gallstone patients have been reported, this was not the case for obese gallstone-free subjects. Despite this, we found the same reduction in nonabsorbable biliary solute concentrations in all the disease study groups, including obese gall-stone-free subjects.

An implication of our finding of markedly impaired fluid absorption leading to a total lipid concentration of less than 5 g/dl, even in the absence of gallstone disease (25% of our morbidly obese gallstone-free patients), is that, in the absence of cystic duct obstruction and /or chronic inflammatory gallbladder sclerosis with atrophy, the exclusion criterion in clinical studies of a totat lipid concentration of less than 5 g/dl and /or of nonopacification of the gallbladder at oral cholecystography is no longer necessary.