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Journal of Lipid Research, Vol. 46, 1491-1501, July 2005
Copyright © 2005 by American Society for Biochemistry and Molecular Biology
Department of Anatomy and Cell Biology, and Pediatrics, SUNY Downstate Medical Center, Brooklyn, NY
Published, JLR Papers in Press, April 16, 2005. DOI 10.1194/jlr.M500023-JLR200
1 To whom correspondence should be addressed. e-mail: Mahmood.hussain{at}downstate.edu
Apolipoprotein B (apoB)-dependent and apoB-independent pathways for cholesterol transport have been described in cultured cells. Here, we show that the apoB-independent pathway involves apoA-I-containing high density lipoproteins (HDLs). Cholesterol secretion by the HDLs, but not by the apoB pathway, was significantly reduced in primary enterocytes isolated from chow- and cholesterol-fed apoA-I–/– mice. These enterocytes were capable of cholesterol efflux when apoA-I was provided extracellularly. In apoA-I–/– mice, the absorption of a bolus of cholesterol was similar in control and apoA-I–/– mice fed chow or high-cholesterol diet. However, short-term studies revealed that cholesterol absorption was occurring over longer lengths of the intestine, and cholesterol but not triglyceride transport to the plasma and liver in chow- and cholesterol-fed apoA-I–/– mice was significantly reduced.
These studies indicate that in apoA-I deficiency, there is a delay in cholesterol absorption, but cholesterol is eventually absorbed because of the compensatory apoB pathway. Nonetheless, long-term studies involving multiple feedings showed significant reduction in cholesterol absorption after 4 days. We propose that multiple compensatory mechanisms ensure efficient cholesterol absorption in mice.
Abbreviations: ABCA1, ATP binding cassette protein A1; apoB, apolipoprotein B; HDL, high density lipoprotein; OA, oleic acid; TC, taurocholate
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