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A high fat diet induces glucose intolerance and decreases GLUT4 and estrogen receptor alpha in adipose tissue of female rats
Author(s) -
Gorres Brittany K,
Bomhoff Gregory L,
Gupte Anisha A,
Geiger Paige C
Publication year - 2010
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.24.1_supplement.821.1
Subject(s) - glut4 , medicine , endocrinology , adipose tissue , ovariectomized rat , type 2 diabetes , estrogen , glucose transporter , insulin resistance , skeletal muscle , glucose uptake , biology , chemistry , diabetes mellitus , insulin
Clinical studies suggest that postmenopausal women are at an increased risk for type 2 diabetes (T2D). While estrogen replacement therapy (ERT) can ameliorate this risk, the molecular mechanisms of estrogen's beneficial effects remain unknown. We hypothesize that a HF diet decreases ERα and GLUT4 in adipose tissue, leading to a decrease in whole body glucose tolerance. Five month old rats were fed a chow (10% fat) or HF (60% fat) diet for 6 weeks, and a subset of animals from each diet group was ovariectomized (OVX) or sham OVX (intact ovaries). Our results show that a HF diet increases abdominal fat, decreases GLUT4 protein in adipose tissue, and decreases whole body glucose tolerance. In addition, a HF diet and OVX alone and in combination decreased ERα protein levels in adipose tissue, and there was a trend towards decreased GLUT4 protein in adipose tissue with OVX, suggesting that a decrease in ERα either by a HF diet and/or OVX may decrease GLUT4. A HF diet and OVX alone and in combination decreased ERβ in the soleus muscle, suggesting that ERβ may play a role in skeletal muscle glucose regulation. Our study shows that the decrease in whole body glucose tolerance due to a short‐term HF diet results from decreased GLUT4 protein in adipose tissue. Furthermore, this decrease in GLUT4 may be modulated by a decrease in ERα. ERT may benefit postmenopausal women by increasing GLUT4 protein through ERα.