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| Research article summary (published 29 Nov 2009): |
Overexpression of low-density lipoprotein receptor and lipid accumulation in intestinal polyps in Min mice.
Full Abstract
Apc-deficient Min mice feature low expression of lipoprotein lipase (LPL), high concentration of serum triglyceride (TG), fatty change of the liver and large numbers of intestinal polyps. We have reported that induction of LPL expression reduces serum lipid, especially TG, improves fatty change of the liver and inhibits intestinal polyp formation in the mice. In this study, fatty change/lipid accumulation in intestinal mucosa and polyps in Min mice were analyzed by Oil-red O staining and electron microscopy. A number of large lipid droplets were found in the epithelia of the upper part of polyps. On the other hand, small lipid droplets were only slightly observed at the tip of the villi in non-tumoros parts of the small intestine of Min mice and in the villi of wild-type mice. Moreover, low-density lipoprotein receptor (LDLR) was overexpressed in the area where lipid droplets were observed. The expression levels of LDLR mRNA in the intestinal polyps of Min mice were approximately 3 times higher compared to those in the non-tumoros parts. Remarkable expression of cyclooxygenase-2 was mainly distributed in stromal cells and some in epithelial cells. It is speculated that lipid accumulation in the intestinal polyps may play an important role in intestinal polyp formation in Apc-deficient mice.
Author information
Author/s: Mutoh, Michihiro (M); Komiya, Masami (M); Teraoka, Naoya (N); Ueno, Toshiya (T); Takahashi, Mami (M); Kitahashi, Tsukasa (T); Sugimura, Takashi (T); Wakabayashi, Keiji (K);
Affiliation: Cancer Prevention Basic Research Project, National Cancer Center Research Institute, Tokyo, Japan. mimutoh(-atsign-)ncc.go.jp
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't
Journal: International journal of cancer. Journal international du cancer (Int J Cancer), published in United States. (Language: eng)
Reference: 2009-Dec; vol 125 (issue 11) : pp 2505-10
Dates: Created 2009/10/05; Completed 2009/11/06;
PMID: 19544529, status: MEDLINE (last retrieval date: 11/6/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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