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Excess dietary energy intake and estrogen‐deprivation modulate adiposity‐related proinflammatory events in C57BL/6J mice
Author(s) -
Kim Jin,
Kim Min-Young,
Park Jinah,
Bak Youn-Kyung
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb446
Subject(s) - medicine , endocrinology , leptin , adiponectin , adipokine , adipose tissue , proinflammatory cytokine , ovariectomized rat , estrogen , foxo1 , protein kinase b , inflammation , obesity , biology , insulin resistance , phosphorylation , biochemistry
Postmenopausal weight gain is related to the development of breast cancer. The aim of this study was to explain the effects of excess body fat accumulation and/or estrogen deprivation on adiposity‐related pro‐inflammatory events. C57BL/6J female mice ovariectomized (OVX) or sham‐operated (SH) at 5 wk of age were fed with normal diet (ND, 15% fat as energy) or high fat diet (HD, 45% fat as energy) for 12 wk. Body and adipose tissue weight were significantly higher in OVX mice. High fat diet significantly increased the level of circulating insulin while the adiponectin level was decreased. The leptin level was significantly increased by OVX. There was no significant difference in the expression of PPAR‐¥á and SREBP1c mRNA in the liver. However, the expression of muscle Akt, phosphorylated Akt, FOXO1, and phosphorylated FOXO1 was higher in OVX+HD mice indicating possible muscle protein degradation. Adipose tissue leptin and TNF‐¥á mRNA expression were increased in OVX+HD mice. These results indicate that both estrogen deficiency and excess energy intake regulate systemic inflammation by modulating the production of major adipokines. This research was supported by Basic Science Research Program through the National Research Foundation of Korea(NRF) funded by the Ministry of Education, Science and Technology(20110011669)