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Specific binding of high density lipoprotein (HDL3) is not related to sterol synthesis in rat intestinal mucosa.

作者信息

Kagami A, Fidge N H, Nestel P J

出版信息

J Lipid Res. 1985 Jun;26(6):705-12.

PMID:2993463
Abstract

There is good evidence that high density lipoprotein (HDL) is involved in the flux of cholesterol into the cells of some organs and out of the cells of other tissues. Because we have previously found that HDL is bound specifically by mucosal cells of the small intestine, we have examined the possibility that this was associated with regulation of cholesterol flux. We have, therefore, compared the specific binding of 125I-labeled HDL3 with cholesterol synthesis in mucosal cells obtained from rats that had been treated to alter intestinal cholesterol metabolism. The rate of sterol synthesis measured in tissue slices, by the incorporation of [3H]water into sterols, was altered up to fivefold by treatment with cholestyramine (to induce bile salt loss), by surformer treatment (to reduce absorption of cholesterol), and by biliary diversion. Yet the capacity of mucosal cells to bind, internalize, and degrade 125I-labeled HDL3 was unchanged. Cholesterol feeding influenced neither the interaction of 125I-labeled HDL3 with cells nor the rate of sterol synthesis. Furthermore, the interactions of 125I-labeled HDL3 with mucosal cells isolated from the proximal and distal halves of the intestine or between the upper and lower villus cells were similar, despite differences in sterol synthesis. These data suggest that, in rat intestine, the specific binding of HDL is not related to sterol synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

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引用本文的文献

1
Cholesterol synthesis and high density lipoprotein uptake are regulated independently in rat small intestinal epithelium.大鼠小肠上皮细胞中胆固醇合成和高密度脂蛋白摄取是独立调节的。
Gut. 1994 Mar;35(3):343-6. doi: 10.1136/gut.35.3.343.
2
Cholesterol feeding to rats does not modulate the expression of binding sites for HDL on liver membranes.给大鼠喂食胆固醇不会调节肝细胞膜上高密度脂蛋白结合位点的表达。
Experientia. 1986 Oct 15;42(10):1155-7. doi: 10.1007/BF01941290.