Linked Life Data

14522940

Source:http://linkedlifedata.com/resource/pubmed/id/14522940

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18
pubmed:dateCreated
2003-10-2
pubmed:abstractText
Epidemiological studies have shown a positive association of colon cancer with hyperlipidemia. Furthermore, signaling generated by peroxisome proliferator-activated receptor (PPAR) alpha and gamma ligands, suggested to be candidate tumor preventive agents, has been shown to lower serum triglyceride levels. In the present study, we assessed hyperlipidemia in Apc-deficient mice, model animals for human familial adenomatous polyposis, and examined the effects of pioglitazone and bezafibrate, respectively, PPARgamma and PPARalpha agonists, on both hyperlipidemia and intestinal polyposis. Serum lipid levels in Apc(1309) mice and Min mice from 6 to 15 weeks of age were measured. Although serum levels of triglyceride and cholesterol were low in both Apc(1309) and wild-type mice at 6 weeks, triglycerides were elevated 10-fold in Apc(1309) mice by the age of 12 weeks but not in their wild-type counterparts. Cholesterol was also increased significantly, and marked centrilobular-restricted steatosis was observed in the livers of aged Apc(1309) mice. Similar findings were observed for Min mice at 15 weeks of age. Moreover, lipoprotein lipase mRNA levels in the liver and small intestine of Apc(1309) and Min mice were demonstrated to be lower than those in wild-type mice. Treatment of Apc(1309) mice with 100 and 200 ppm pioglitazone or bezafibrate for 6 weeks from 6 weeks of age caused dose-dependent reduction in serum triglycerides and cholesterol, along with reduction in the numbers of intestinal polyps to 67% of the control value. The present study clearly demonstrated a hyperlipidemic state in Apc gene-deficient mice and a potential of PPARalpha and PPARgamma ligands to suppress both hyperlipidemia and polyp formation. Hyperlipidemia in these mice may thus be associated with their intestinal lesion development.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
63
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6090-5
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:14522940-Age Factors, pubmed-meshheading:14522940-Animals, pubmed-meshheading:14522940-Bezafibrate, pubmed-meshheading:14522940-Cholesterol, pubmed-meshheading:14522940-Fatty Acids, Nonesterified, pubmed-meshheading:14522940-Genes, APC, pubmed-meshheading:14522940-Hyperlipidemias, pubmed-meshheading:14522940-Intestinal Polyposis, pubmed-meshheading:14522940-Intestine, Small, pubmed-meshheading:14522940-Ligands, pubmed-meshheading:14522940-Lipoprotein Lipase, pubmed-meshheading:14522940-Liver, pubmed-meshheading:14522940-Mice, pubmed-meshheading:14522940-Mice, Inbred C57BL, pubmed-meshheading:14522940-Mice, Knockout, pubmed-meshheading:14522940-RNA, Messenger, pubmed-meshheading:14522940-Receptors, Cytoplasmic and Nuclear, pubmed-meshheading:14522940-Thiazolidinediones, pubmed-meshheading:14522940-Transcription Factors, pubmed-meshheading:14522940-Triglycerides
pubmed:year
2003
pubmed:articleTitle
Concomitant suppression of hyperlipidemia and intestinal polyp formation in Apc-deficient mice by peroxisome proliferator-activated receptor ligands.
pubmed:affiliation
Cancer Prevention Division, National Cancer Center Research Institute, Tokyo, Japan. nniho@gan2.ncc.go.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't