Biliary lipid secretion and bile composition after acute and chronic interruption of the enterohepatic circulation in the Rhesus monkey. IV. Primate biliary physiology.
Bile salts and phospholipids are both required to solubilize biliary cholesterol. Since interruption of the enterohepatic circulation (EHC) depletes bile of bile salts, we have examined in the rhesus monkey the effects of controlled interruption of the EHC on biliary secretion of bile salt, phospholipid, and cholesterol and on the relative proportions of these components in bile. Immediately after complete interruption of the EHC, bile secretion and bile composition remained normal for 2-3 hr. During the next 3 hr, however, secretion of all components decreased. Bile salt decreased to a greater extent than phospholipid and cholesterol, and the bile was now supersaturated with cholesterol. 12-24 hr after interruption of the EHC, a new steady state was reached in which there was a relative deficiency of bile salt and a relative increase in phospholipid and cholesterol. The resulting bile, although somewhat more saturated with cholesterol, was not supersaturated with cholesterol but was stable with respect to cholesterol solubility. Thus, bile instability conducive to gallstone formation occurs transiently within hours after interruption of the EHC. Prolonged large interruptions in the steady state animal also produce a relative bile salt deficiency, but in this situation cholesterol remains soluble in the bile of these animals because there occurs a concomitant relative increase in phospholipid. When the EHC was only partially interrupted, secretion rates and the relative concentration of bile salt, phospholipid, and cholesterol did not change significantly from control values until more than 20% of the bile was diverted. Modest changes in the relative composition of bile occurred when 33 and 66% of the bile was diverted, and these changes were very similar to those produced by resection of the distal small bowel.
D000818:Animals; D001646:Bile / Q000032:analysis*; D001647:Bile Acids and Salts / Q000378:metabolism; D002784:Cholesterol / Q000378:metabolism; D000882:Haplorhini; D007421:Intestine, Small / Q000502:physiology*; D050356:Lipid Metabolism; D008099:Liver / Q000502:physiology*; D008954:Models, Biological; D010713:Phosphatidylcholines; D010743:Phospholipids / Q000378:metabolism; D012636:Secretory Rate; D012995:Solubility
D001647:Bile Acids and Salts; D010713:Phosphatidylcholines; D010743:Phospholipids; D002784:Cholesterol