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

PERELLÓ M,; CONSOLE G; GAILLARD RC; SPINEDI E

ENDOCRINE

HUMANA PRESS INC

Año: 2010 p. 497 - 506

0969-711X

The hypothalamic damage induced by neonataltreatment with monosodium L-glutamate (MSG) inducesseveral metabolic abnormalities, resulting in a rat hyperleptinemic–hyperadipose phenotype. This study was conductedto explore the impact of the neonatal MSGtreatment, in the adult (120 days old) female rat on: (a) thein vivo and in vitro mineralocorticoid responses to ACTHand angiotensin II (AII); (b) the effect of leptin on ACTHandAII-stimulated mineralocorticoid secretions by isolatedcorticoadrenal cells; and (c) abdominal adiposity characteristics.Our data indicate that, compared with age-matchedcontrols, MSG rats displayed: (1) enhanced andreduced mineralocorticoid responses to ACTH and AIItreatments, respectively, effects observed in both in vivoand in vitro conditions; (2) adrenal refractoriness to theinhibitory effect of exogenous leptin on ACTH-stimulatedaldosterone output by isolated adrenocortical cells; and (3)distorted omental adiposity morphology and function. Thisstudy supports that the adult hyperleptinemic MSG femalerat is characterized by enhanced ACTH-driven mineralocorticoidfunction, impaired adrenal leptin sensitivity, anddisrupted abdominal adiposity function. MSG rats couldcounteract undesirable effects of glucocorticoid excess, bydeveloping a reduced AII-driven mineralocorticoid function.Thus, chronic hyperleptinemia could play a protectiverole against ACTH-mediated allostatic loads in the adrenalleptin resistant, MSG female rat phenotype.