期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2000
卷号：97
期号：23
页码：12729-12734
DOI：10.1073/pnas.97.23.12729
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Estrogen regulates the amount of white adipose tissue (WAT) in females, but its role in males and whether WAT effects involve estrogen receptor- (ER) or ER{beta} were unclear. We analyzed the role of ER in WAT and brown adipose tissue by comparing these tissues in wild-type (WT) and ER-knockout (ERKO) male and female mice. Brown adipose tissue weight was similar in ERKO and WT males at all ages. Progressive increases in WAT were seen in ERKO males with advancing age. Epididymal, perirenal, and inguinal WAT weighed 139-185% more in ERKO than in WT males by 270-360 days of age. Epididymal and perirenal adipocyte size was increased 20% in ERKO males. Adipocyte number was 82-168% greater in fat pads of ERKO vs. WT males. Compared with WT, 90-day-old ERKO females had increases in fat pad weights (54-103%), adipocyte size, and number. Both ERKO males and females had insulin resistance and impaired glucose tolerance, similar to humans lacking ER or aromatase. Energy intake was equal in WT and ERKO males, indicating that obesity was not induced by hyperphagia. In contrast, energy expenditure was reduced by 11% in ERKO compared with WT males, indicating that altered energy expenditure may be important for the observed obesity. In summary, ER absence causes adipocyte hyperplasia and hypertrophy, insulin resistance, and glucose intolerance in both sexes. These results are evidence that estrogen/ER signaling is critical in female and male WAT; obesity in ERKO males involves a mechanism of reduced energy expenditure rather than increased energy intake.
