Effects of peroxisome proliferator-activated receptor δ on placentation, adiposity, and colorectal cancer

被引：492

作者：

Barak, Y

Liao, D

He, WM

Ong, ES

Nelson, MC

Olefsky, JM

Boland, R

Evans, RM ^{[1
]}

机构：

[1] Univ Calif San Diego, Sch Med, Dept Med & Canc Ctr, La Jolla, CA 92093 USA

[2] Salk Inst Biol Studies, Gene Express Lab, La Jolla, CA 92037 USA

[3] Salk Inst Biol Studies, Howard Huges Med Inst, La Jolla, CA 92037 USA

[4] Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA

[5] San Diego Vet Affairs, Med Ctr, Div Endocrinol & Metab, La Jolla, CA 92093 USA

[6] Whittier Diab Inst, La Jolla, CA 92093 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2002年 / 99卷 / 01期

关键词：

D O I：

10.1073/pnas.012610299

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Targeting of the nuclear prostaglandin receptor peroxisome proliferator-activated receptor delta (PPARdelta) by homologous recombination results in placental defects and frequent (>90%) midgestation lethality. Surviving PPARdelta(-/-) mice exhibit a striking reduction in adiposity relative to wild-type levels. This effect is not reproduced in mice harboring an adipose tissue-specific deletion of PPARdelta, and thus likely reflects peripheral PPARdelta functions in systemic lipid metabolism. Finally, we observe that PPARdelta is dispensable for polyp formation in the intestine and colon of APC(min) mice, inconsistent with its recently proposed role in the establishment of colorectal tumors. Together, these observations reveal specific roles for PPARdelta in embryo development and adipocyte physiology, but not cancer.

引用

页码：303 / 308

页数：6

共 28 条

[1] REGULATION OF MDM2 EXPRESSION BY P53 - ALTERNATIVE PROMOTERS PRODUCE TRANSCRIPTS WITH NONIDENTICAL TRANSLATION POTENTIAL [J].