Postprandial appearance of dietary deuterated cholesterol in the chylomicron fraction and whole plasma in healthy subjects
- PMID: 8669413
- DOI: 10.1093/ajcn/64.1.47
Postprandial appearance of dietary deuterated cholesterol in the chylomicron fraction and whole plasma in healthy subjects
Abstract
This study examined the appearance of dietary cholesterol in the chylomicron fraction (chylomicrons plus chylomicron remnants) and whole plasma in healthy normolipidemic subjects during a 0-7-h postprandial period. Six adult males were given two diet sequences in random order: a low-fiber diet (standard Western diet for 14 d) followed by a labeled low-fiber test meal or a fiber-supplemented diet (40 g oat bran/d for 14 d) followed by a labeled oat bran (40 g) test meal. The test meals provided 192.5 mg cholesterol, including 80.1 mg octadeuterated cholesterol. Fasting and hourly postmeal blood samples were obtained for 7 h. Isotopic cholesterol ratios [tracer:(tracer+native cholesterol)] were determined by gas chromatography-mass spectrometry. Chylomicron triacylglycerol and cholesterol concentrations peaked after 2-3 h and returned to baseline after 7 h. After the low-fiber test meal, the isotopic cholesterol ratio continuously increased until 7 h in the chylomicron fraction (4.2 +/- 1.2 x 10(-3)) and whole plasma (1.04 +/- 0.39 x 10(-3)). At 7 h postprandial, the maximum dietary cholesterol concentration in the chylomicron fraction and plasma cholesterol was 1 in 99 and 1 in 397 cholesterol molecules, respectively. No marked differences were obtained after the high-fiber sequence compared with the low-fiber one; there was a comparable isotopic cholesterol ratio and concentration in the chylomicron fraction and a slightly lower (-44%, P < 0.10) 0-7 h area under the curve whole-plasma deuterated cholesterol concentration. Thus, dietary cholesterol supplied as a single meal does not simultaneously appear in the chylomicron fraction postprandially with endogenous cholesterol and triacylglycerols and fiber feeding does not markedly alter this process in healthy normolipidemic humans.
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