-
Thrombosis Research 02/2008; 121(6):769-72. · 2.44 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Esterification of dietary phytosterols and glycerols may affect intestinal absorption of cholesterol and non-cholesterol sterols. We infused plant stanol esters in triacylglycerol (TAG) (F1) and diacylglycerol (DG) (F2) oils, and free plant stanols in F1 and F2 (F3) to the duodenum of healthy human subjects and sampled the contents from the proximal jejunum (PJ). Free and ester sterols were analysed from the infusates, and intestinal contents before and after ultracentrifuge separation of oil, micelle and sediment phases. During the 60-cm intestinal passage, over 40% of plant stanol esters were hydrolysed (P < 0.05) but around 30% of the infused free plant stanols (P < 0.05) and up to 40% of cholesterol (P < 0.05) were esterified in PJ after infusions. TAG in F1 favoured accumulation of plant stanol esters in the oil phase of the PJ aspirates as compared with respective values of F2 and F3 (P < 0.05 for both). About one third of free plant stanols of F3 had been esterified (P < 0.05) and 17% precipitated mainly in free form in the PJ aspirates (P < 0.05 compared with F1 and F2). In conclusion, DG- and TAG-oils had no profound superiority over each other as intestinal carriers regarding hydrolysis/esterification of administered plant stanol esters and cholesterol and their partition in oil, micellar and sediment phases in the PJ. The unesterified plant stanols experienced partial esterification and sedimentation during their intestinal passage, which might influence their biochemical properties in that segment of the gut where cholesterol is absorbed.
Lipids 07/2007; 42(7):603-12. · 2.13 Impact Factor
-
European Journal of Clinical Pharmacology 03/2005; 60(12):905-7. · 2.85 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Properties of the intestinal digestion of the dietary phytosterols, cholesterol and cholestanol, and the mechanisms by which phytosterols inhibit the intestinal absorption of cholesterol in healthy human subjects are poorly known. We have studied the hydrolysis of dietary plant sterol and stanol esters and their subsequent micellar solubilization by determining their concentrations in micellar and oil phases of the jejunal contents. Two liquid formulas with low (formula 1) and high (formula 2) plant stanol concentrations were infused via a nasogastric tube to the descending duodenum of 8 healthy human subjects, and intestinal contents were sampled for gas-liquid chromatographic sterol analysis 60 cm more distally. During the duodenal transit, phytosterol esters were hydrolyzed. This was especially profound for sitostanol, as its esterified fraction per milligram of sitosterol decreased 80% (P < 0.001) in formula 1 and 61% (P < 0.001) in formula 2. Contrary to that, esterified fraction of cholesterol per milligram of sitosterol was increased fourfold (P < 0.001) in formula 1 and almost sixfold (P < 0.001) in formula 2, whereas that of cholestanol remained unchanged. Percentages of esterified sterols and stanols in total intestinal fluid samples were higher after the administration of formula 2 than of formula 1. Esterified cholesterol and stanols accumulated in the oil phase, and free stanols replaced cholesterol in the micellar phase. At high intestinal plant stanol concentrations, cholesterol looses its micellar solubility possibly by replacement of its free fraction in the micellar phase by hydrolyzed plant stanols, which leads to a decreased intestinal absorption of cholesterol.
AJP Gastrointestinal and Liver Physiology 06/2002; 282(6):G1009-15. · 3.43 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Cholesterol absorption, elimination, and synthesis, and low-density lipoprotein (LDL) and high density lipoprotein (HDL) kinetics were studied in patients with mild to severe primary biliary cirrhosis (PBC) (n = 16) to show how this cholestatic disease modified cholesterol and lipoprotein metabolism as compared with healthy controls (n = 50). Serum total and lipoprotein cholesterol and triglyceride levels were similar in the two groups, but in PBC, especially in severe forms, very low density lipoprotein (VLDL) was rich in apoprotein (apo) B and cholesterol and low in triglycerides, whereas LDL was rich in triglycerides and low in triglycerides and low in esterified cholesterol, and HDL was enriched by surface lipids, phospholipids, and free cholesterol. In severe PBC, the fractional catabolic rate (FCR) for LDL apo B was reduced. The transport rate (TR) for LDL apo B was unaffected and it tended to correlate with the LDL apo B and LDL cholesterol levels in PBC, whereas in the controls the LDL apo B concentration was regulated by both the FCR and TR, and LDL cholesterol was regulated only by FCR. FCR for apo A-I in HDL was unaltered in PBC, but TR for apo A-I was reduced in the severe cases. Cholesterol absorption efficiency was significantly reduced in PBC (14.5 ± 3.0% in severe PBC and 34.0 ± 2.5% in mild PBC vs. 47.4 ± 1.4% in the controls, respectively). Bile acid synthesis and cholesterol transport were significantly diminished in PBC, but, even in a case with severe PBC and low basal absorption efficiency and synthesis of cholesterol, lowering of LDL cholesterol by combined inhibition of hydroxymethyl-glutaryl-coenzyme A reductase and cholesterol absorption, removal of LDL apo B could still be upregulated. The significant interrelations between the LDL apo B level, cholesterol absorption efficiency and synthesis, and LDL apo B kinetics, observed in the controls, were lacking in PBC, suggesting that cholestasis and hepatic parenchymal cell dysfunction modified the relationship between cholesterol and lipoprotein metabolism so that treatment of hypercholesterolemia and bile acid-related itching might not be constantly successful. (Hepatology 1995;21:89–95).
Hepatology 12/1994; 21(1):89 - 95. · 11.66 Impact Factor
