Analysis of angiotensin II- and ACTH-driven mineralocorticoid functions and omental adiposity in a non-genetic, hyperadipose female rat phenotype.

Details

Serval ID
serval:BIB_32B18B1898B7
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Analysis of angiotensin II- and ACTH-driven mineralocorticoid functions and omental adiposity in a non-genetic, hyperadipose female rat phenotype.
Journal
Endocrine
Author(s)
Perelló M., Cónsole G., Gaillard R.C., Spinedi E.
ISSN
1559-0100 (Electronic)
ISSN-L
1355-008X
Publication state
Published
Issued date
06/2010
Peer-reviewed
Oui
Volume
37
Number
3
Pages
497-506
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Abstract
The hypothalamic damage induced by neonatal treatment with monosodium L -glutamate (MSG) induces several metabolic abnormalities, resulting in a rat hyperleptinemic-hyperadipose phenotype. This study was conducted to explore the impact of the neonatal MSG treatment, in the adult (120 days old) female rat on: (a) the in vivo and in vitro mineralocorticoid responses to ACTH and angiotensin II (AII); (b) the effect of leptin on ACTH- and AII-stimulated mineralocorticoid secretions by isolated corticoadrenal cells; and (c) abdominal adiposity characteristics. Our data indicate that, compared with age-matched controls, MSG rats displayed: (1) enhanced and reduced mineralocorticoid responses to ACTH and AII treatments, respectively, effects observed in both in vivo and in vitro conditions; (2) adrenal refractoriness to the inhibitory effect of exogenous leptin on ACTH-stimulated aldosterone output by isolated adrenocortical cells; and (3) distorted omental adiposity morphology and function. This study supports that the adult hyperleptinemic MSG female rat is characterized by enhanced ACTH-driven mineralocorticoid function, impaired adrenal leptin sensitivity, and disrupted abdominal adiposity function. MSG rats could counteract undesirable effects of glucocorticoid excess, by developing a reduced AII-driven mineralocorticoid function. Thus, chronic hyperleptinemia could play a protective role against ACTH-mediated allostatic loads in the adrenal leptin resistant, MSG female rat phenotype.

Keywords
Adiposity/drug effects, Adrenal Cortex/drug effects, Adrenal Cortex/metabolism, Adrenocorticotropic Hormone/pharmacology, Aldosterone/blood, Aldosterone/metabolism, Angiotensin II/pharmacology, Animals, Animals, Newborn, Female, Hypothalamus/drug effects, Omentum/cytology, Phenotype, Rats, Rats, Sprague-Dawley, Sodium Glutamate/toxicity
Pubmed
Web of science
Create date
18/05/2010 15:23
Last modification date
20/08/2019 13:18
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