| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1992621 | The Journal of Steroid Biochemistry and Molecular Biology | 2009 | 8 Pages |
Oleoyl-estrone (OE) elicits a decrease in body fat, which is blocked by glucocorticoids. In order to analyze this counterregulatory effect, we studied the effects of oral OE on adrenalectomized female rats simultaneously receiving corticosterone (subcutaneous pellets). Circulating corticosteroids, liver glycogen, lipids and the expressions in whole liver, soleus muscle, interscapular brown adipose tissue (BAT), and the inguinal and periovaric white adipose tissue (WAT) of genes controlling lipid metabolism were analyzed. Corticosterone reversed OE lipid mobilization, storing fat in liver and subcutaneous WAT. This was not simply the predominance of corticosteroid enhancement of lipogenesis against OE inhibition, but a synergy to enhance lipogenesis. Periovaric WAT showed a different effect, with corticosterone inhibiting OE arrest of lipogenic gene expressions. The data presented suggests that interaction of OE and glucocorticoids (and the metabolic response) depends on the organ or WAT site; there was a direct relationship on the direction and extent of change of SREBP1c expression with those of important energy and lipid handling genes. Our results confirm that corticosterone blocks – and even reverses – OE effects on body lipids in a dose-dependent way, a process mediated, at least in part, by modulation of SREBP1c expression.
