ALDOSTERONE AND DEXAMETHASONE BOTH STIMULATE ENERGY ACQUISITION WHEREAS ONLY THE GLUCOCORTICOID ALTERS ENERGY-STORAGE

Citation
P. Santana et al., ALDOSTERONE AND DEXAMETHASONE BOTH STIMULATE ENERGY ACQUISITION WHEREAS ONLY THE GLUCOCORTICOID ALTERS ENERGY-STORAGE, Endocrinology, 136(5), 1995, pp. 2214-2222
Citations number
42
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
00137227
Volume
136
Issue
5
Year of publication
1995
Pages
2214 - 2222
Database
ISI
SICI code
0013-7227(1995)136:5<2214:AADBSE>2.0.ZU;2-C
Abstract
Corticosteroids stimulate and insulin inhibits energy acquisition (foo d intake); conversely, corticosteroids inhibit and insulin stimulates energy storage (body weight gain). Thus, together these hormones media te long-term energy balance. This study tested whether the stimulatory action of corticosteroids on food intake was mediated by association with high affinity mineralocorticoid receptors (MRs) or lower affinity glucocorticoid receptors (GRs). Young male rats were adrenalectomized (ADX) and given vehicle (control) or streptozotocin (diabetic); subgr oups of rats were infused with vehicle, aldosterone (Aldo, an MR agoni st in vivo), dexamethasone (Dex, a GR agonist in vivo), or Aldo&Dex fo r the 5 days after ADX. Sham-ADX rats were included. Food intake, body weight gain, and epididymal white adipose and interscapular brown adi pose tissue stores were weighed. ADX decreased food intake by approxim ately 24%, and food intake was not increased by diabetes as it was in sham-ADX rats. In control ADX rats, Dex, but not Aldo, stimulated insu lin, and food intake was not significantly affected by either hormone; together, Aldo and Dex restored insulin and food intake to sham-ADX r ats. Food intake in diabetic ADX rats was significantly increased by e ach treatment (ADX < Aldo < Dex < Aldo&Dex = sham). Aldo increased bod y weight through an increase in fluid volume (estimated by decreased p lasma protein concentration); however, fat stores were not different f rom ADX. Dex reduced body weight in control rats but maintained fat st ores; in diabetic rats, body weight and fat stores were less than or s imilar to ADX. We conclude that: 1) corticosteroids, acting through as sociation with both MRs and GRs, stimulate food intake; 2) insulin cou nteracts the GR-mediated stimulation of food intake in control rats; a nd 3) Dex and insulin, which is stimulated by Dex, selectively maintai n or increase body fat stores, probably at the expense of protein stor es.