Factors affecting intestinal absorption of cholesterol and plant sterols and stanols.
Various factors affect intestinal absorption of cholesterol and plant sterols and stanols. Plant sterols and stanols are generally less absorptive than cholesterol. Differential absorption rates among various plant sterols and stanols have been also reported. Although it was suggested that differential absorption among cholesterol and various plant sterols was determined by difference in excretion rates of sterols and stanols through ATP-binding cassette transporter (ABC) G5/ABCG8 of intestinal cells, our study suggests that affinity for and solubility in bile salt micelles can be important determinants for differential absorption of plant sterols and stanols. It was also suggested that plant sterols were transiently incorporated into intestinal cells and then excreted to intestinal lumen through ABCG5/ABCG8. However, in a rat study, transient incorporation of sitosterol into intestinal cells was not observed, suggesting that sitosterol is differentiated from cholesterol at the incorporation site of intestinal cells. It is well established that plant sterols inhibit intestinal absorption of cholesterol and exert a hypocholesterolemic activity. Plant sterols are solubilized in bile salt micelles as cholesterol. Our study clearly showed that because the sterol-solubilizing capacity of bile salt micelles was limited, plant sterols solubilized in micelles reduced the solubility of cholesterol. This can be the major cause of inhibition of cholesterol absorption by plant sterols. Pancreatic cholesterol esterase accelerates intestinal absorption of unesterified cholesterol. Although it was suggested that cholesterol esterase accelerated esterification of cholesterol incorporated into intestinal cells and acted as a transporter at the surface of intestinal cells, our research revealed that the accelerated cholesterol absorption was caused by hydrolysis of phosphatidylcholine in bile salt micelles. It is thought that hydrolysis of phosphatidylcholine reduces the affinity of cholesterol for the micelles and accelerates the incorporation of cholesterol released from the micelles into intestinal cells.
Laboratory of Food and Biomolecular Science, Graduate School of Agricultural Science, Tohoku University.
Ikuo
I
Ikeda
D000071018:ATP Binding Cassette Transporter, Subfamily G, Member 5; D000071019:ATP Binding Cassette Transporter, Subfamily G, Member 8; D018528:ATP-Binding Cassette Transporters / Q000378:metabolism; D000818:Animals; D000924:Anticholesteremic Agents; D001647:Bile Acids and Salts / Q000378:metabolism; D002784:Cholesterol / Q000378:metabolism*; D004951:Esterification / Q000187:drug effects; D006801:Humans; D006868:Hydrolysis; D007408:Intestinal Absorption / Q000187:drug effects / Q000502:physiology*; D007413:Intestinal Mucosa / Q000378:metabolism*; D007422:Intestines / Q000166:cytology; D008074:Lipoproteins / Q000378:metabolism; D008823:Micelles; D010713:Phosphatidylcholines / Q000378:metabolism; D010840:Phytosterols / Q000378:metabolism* / Q000494:pharmacology; D051381:Rats; D012855:Sitosterols / Q000378:metabolism*; D012995:Solubility / Q000187:drug effects; D002787:Sterol Esterase / Q000494:pharmacology / Q000502:physiology
C416945:ABCG5 protein, human; C416946:ABCG8 protein, human; D000071018:ATP Binding Cassette Transporter, Subfamily G, Member 5; D000071019:ATP Binding Cassette Transporter, Subfamily G, Member 8; D018528:ATP-Binding Cassette Transporters; D000924:Anticholesteremic Agents; D001647:Bile Acids and Salts; D008074:Lipoproteins; D008823:Micelles; D010713:Phosphatidylcholines; D010840:Phytosterols; D012855:Sitosterols; C407042:plant stanol ester; C025473:gamma-sitosterol; D002784:Cholesterol; C054784:bile salt-stimulated lipase; D002787:Sterol Esterase