Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2007-8-27
pubmed:abstractText
Apc gene-deficient Min and Apc(1309) mice feature a hyperlipidemic state with a markedly low expression level of lipoprotein lipase (LPL) compared to their wild-type counterparts. We previously showed that induction of LPL mRNA by peroxisome proliferator-activated receptor (PPAR) alpha and gamma agonists or an LPL selective inducer suppresses both high serum lipid levels and intestinal polyp formation in these model animals. Since the general cyclooxygenase inhibitor, indomethacin, is known to suppress intestinal tumor development, but not to affect serum lipids, its influence in Min mice was here investigated. Treatment with 2.5, 5 and 10 ppm indomethacin in the diet for 14 weeks from 6 weeks of age caused significant dose-dependent reduction in serum triglycerides, along with a reduction in the numbers of intestinal polyps to 25% of the untreated control value. LPL mRNA levels in the liver were slightly increased by indomethacin treatment. We further performed oligonucleotide microarray analysis and quantitative PCR analysis and found 8 lipid metabolism-related genes, regulated by sterol regulatory element binding protein-1c, to be modulated by indomethacin-treatment in the Min mouse liver. Furthermore, TNFalpha was downregulated. These results indicate that indomethacin might suppress intestinal tumor formation together with a hyperlipidemic state by regulating LPL and other lipid metabolic factors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0020-7136
pubmed:author
pubmed:copyrightInfo
(c) 2007 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
121
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1665-9
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:17546600-Animals, pubmed-meshheading:17546600-Cyclooxygenase Inhibitors, pubmed-meshheading:17546600-DNA, Complementary, pubmed-meshheading:17546600-Dose-Response Relationship, Drug, pubmed-meshheading:17546600-Female, pubmed-meshheading:17546600-Gene Expression Regulation, Enzymologic, pubmed-meshheading:17546600-Hyperlipidemias, pubmed-meshheading:17546600-Hypolipidemic Agents, pubmed-meshheading:17546600-Indomethacin, pubmed-meshheading:17546600-Lipoprotein Lipase, pubmed-meshheading:17546600-Liver, pubmed-meshheading:17546600-Mice, pubmed-meshheading:17546600-Mice, Inbred C57BL, pubmed-meshheading:17546600-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:17546600-Polymerase Chain Reaction, pubmed-meshheading:17546600-RNA, Messenger, pubmed-meshheading:17546600-Sterol Regulatory Element Binding Protein 1, pubmed-meshheading:17546600-Triglycerides
pubmed:year
2007
pubmed:articleTitle
Improvement of hyperlipidemia by indomethacin in Min mice.
pubmed:affiliation
Cancer Prevention Basic Research Project, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't