Linked Life Data

20858763

Source:http://linkedlifedata.com/resource/pubmed/id/20858763

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2010-10-15
pubmed:abstractText
The possibility that dietary vitamin D(3) (VD(3)) exposure inhibits endometrial carcinogenesis in an animal model and modifies the enhanced risk of endometrial carcinoma associated with obesity was investigated. At 4 weeks of age, Pten(+/-) and wild-type mice were each divided into four treatment groups and fed AIN93G control diet, or AIN93G-based diet containing either 25,000 international units of VD(3) per kilogram of diet, 58% fat to induce obesity (high fat), or high fat and 25,000 international units of VD(3) per kilogram of diet. Mice were kept on these diets until they were sacrificed at week 28. Although VD(3) did not affect endometrial cancer risk, it inhibited obesity-induced increase in endometrial lesions. Specifically, high-fat diet increased focal glandular hyperplasia with atypia and malignant lesions from 58% in the control diet-fed Pten(+/-) mice to 78% in obese mice. Dietary VD(3) decreased the incidence of endometrial pathology in obese Pten(+/-) mice to 25% (P < 0.001). VD(3) altered the endometrial expression of 25-hydroxylase, 1?-hydroxylase, and vitamin D receptor in the wild-type and Pten(+/-) mice. Estrogen receptor-? mRNA levels were higher (P < 0.014) and progesterone receptor protein levels in the luminal epithelium were lower (P < 0.04) in the endometrium of control diet-fed Pten(+/-) than wild-type mice, but the expression of these receptors was not affected by the dietary exposures. VD(3) reversed the obesity-induced increase in osteopontin (P < 0.001) and significantly increased E-cadherin expression (P < 0.019) in the endometrium of obese Pten(+/-) mice. Our data confirm the known association between obesity and endometrial cancer risk. Dietary exposure to VD(3) inhibited the carcinogenic effect of obesity on the endometrium. This protective effect was linked to a reduction in the expression of osteopontin and increase in E-cadherin.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1940-6215
pubmed:author
pubmed:copyrightInfo
©2010 AACR.
pubmed:issnType
Electronic
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1246-58
pubmed:meshHeading
pubmed-meshheading:20858763-Animals, pubmed-meshheading:20858763-Blotting, Western, pubmed-meshheading:20858763-Bone Density, pubmed-meshheading:20858763-Cadherins, pubmed-meshheading:20858763-Cholecalciferol, pubmed-meshheading:20858763-Diet, pubmed-meshheading:20858763-Endometrial Neoplasms, pubmed-meshheading:20858763-Endometrium, pubmed-meshheading:20858763-Estrogen Receptor alpha, pubmed-meshheading:20858763-Female, pubmed-meshheading:20858763-Immunohistochemistry, pubmed-meshheading:20858763-Mice, pubmed-meshheading:20858763-Mice, Inbred C57BL, pubmed-meshheading:20858763-Mice, Mutant Strains, pubmed-meshheading:20858763-Obesity, pubmed-meshheading:20858763-Osteopontin, pubmed-meshheading:20858763-PTEN Phosphohydrolase, pubmed-meshheading:20858763-Precancerous Conditions, pubmed-meshheading:20858763-Receptors, Progesterone
pubmed:year
2010
pubmed:articleTitle
Dietary vitamin D exposure prevents obesity-induced increase in endometrial cancer in Pten+/- mice.
pubmed:affiliation
Department of Oncology, Georgetown University, Washington, DC 20057, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, N.I.H., Extramural