Premium
Estrogen Receptor β in Female Adipose Tissue: Impact on Metabolic Dysregulation in a Model of Senescence and Estrogen Deficiency
Author(s) -
Tomicek Nanette J.,
Lancaster Timothy S.,
Korzick Donna H.
Publication year - 2009
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.23.1_supplement.991.6
Subject(s) - endocrinology , medicine , adipose tissue , estrogen , estrogen receptor , adiponectin , senescence , menopause , estrogen receptor alpha , biology , estrogen receptor beta , obesity , insulin resistance , cancer , breast cancer
Background Obesity and associated metabolic risk are increased following menopause and may be associated with disturbances in estrogen receptor (ER) signaling in adipose depots. However, the role of ER subtypes on increasing adiposity with aging remains uninvestigated. Purpose To determine the singular and combined effects of aging and estrogen deficiency on ER levels and to identify dysregulated downstream signaling in adipose tissue of female rats. Methods Visceral adipose tissue was isolated from adult and aged female F344 rats (n = 5‐6/group) with ovaries intact or removed (OVX). Protein levels were assessed with western blotting and circulating estradiol through radioimmunoassay. Results Rat weight increased significantly with both age and OVX and was greatest in aged OVX. ER β levels increased two‐fold in both aged and aged OVX, while ERα decreased in adult OVX only. PPARγ 2 levels were also reduced in aged OVX, in conjunction with a non‐significant increase in adiponectin receptor 1 levels (p = 0.098). Summary These data suggest, for the first time, that alterations in adipose ERβ levels may contribute to obesity and altered metabolic risk with age‐associated estrogen deficiency. ERβ‐mediated suppression of PPARγ 2 may also represent a potential downstream signaling mechanism to exacerbate metabolic risk with post‐menopausal estrogen deficiency via alterations in adiponectin signaling.