| dc.creator | Perelló, Mario Carlos | |
| dc.creator | Console-Avegliano, Gloria Miriam | |
| dc.creator | Gaillard, Rolf C. | |
| dc.creator | Spinedi, Eduardo Julio | |
| dc.date | 2010-04-13 | |
| dc.date | 2022-03-09T17:19:42Z | |
| dc.date.accessioned | 2023-07-15T04:46:55Z | |
| dc.date.available | 2023-07-15T04:46:55Z | |
| dc.identifier | http://sedici.unlp.edu.ar/handle/10915/132244 | |
| dc.identifier | issn:1559-0100 | |
| dc.identifier | issn:1355-008x | |
| dc.identifier.uri | https://repositorioslatinoamericanos.uchile.cl/handle/2250/7470862 | |
| dc.description | 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. | |
| dc.description | Facultad de Ciencias Médicas | |
| dc.description | Comisión de Investigaciones Científicas de la provincia de Buenos Aires | |
| dc.format | application/pdf | |
| dc.format | 497-506 | |
| dc.language | en | |
| dc.rights | http://creativecommons.org/licenses/by/4.0/ | |
| dc.rights | Creative Commons Attribution 4.0 International (CC BY 4.0) | |
| dc.subject | Ciencias Médicas | |
| dc.subject | Hypothalamic obesity | |
| dc.subject | Hypophagia | |
| dc.subject | Mineralocorticoid | |
| dc.subject | Omental adiposity | |
| dc.subject | Glucocorticoid | |
| dc.subject | Leptin | |
| dc.subject | Insulin | |
| dc.title | Analysis of angiotensin II- and ACTH-driven mineralocorticoid functions and omental adiposity in a non-genetic, hyperadipose female rat phenotype | |
| dc.type | Articulo | |
| dc.type | Articulo | |
