title: Impact of transient correction of increased adrenocortical activity in hypothalamo-damaged, hyperadipose female rats.
abstract: OBJECTIVE
  To explore the effects of transient correction of enhanced corticoadrenal activity in monosodium L-glutamate (MSG)-damaged female rats on peripheral insulin sensitivity and in vitro retroperitoneal (RP) adipocyte function.
  
  
  METHODS
  A dose of 4 mg/g body weight (BW) of MSG or vehicle (CTR) was i.p. injected, once every 2 days, between days 2 and 10 of age, in female rats. Intact and 21 day-operated (sham or adrenal enucleation (AE)) rats from both (CTR and MSG) groups were used for experimentation on day 120 of age. Circulating levels of several hormones, in basal and after i.v. high-glucose load conditions, and RP adiposity morphology and function were then evaluated.
  
  
  RESULTS
  MSG rats developed increased adrenocortical function, hyperadiposity, hyperleptinemia, hyperinsulinemia and decreased peripheral insulin sensitivity. These characteristics were fully reversed after transient correction of corticoadrenal hyperactivity induced by AE. In addition, in vitro experimentation with isolated RP adipocytes indicated that cells from intact MSG animals displayed decreased sensitivity to insulin and dexamethasone stimulation of leptin secretion. Interestingly, adipocyte dysfunction in MSG rats was fully abrogated after AE-induced transient correction of insulinemia, leptinemia and adrenocortical activity. Importantly, the reversion of these metabolic abnormalities, induced by AE for 21 days, in MSG animals did occur, despite no significant changes in BW values.
  
  
  CONCLUSIONS
  Our results support that the changes in adipocyte characteristics and peripheral insulin resistance, developed in this pseudo-obese female rat model, are mainly due to increased glucocorticoid production. Importantly, appropriate correction of the enhanced adrenocortical activity fully reversed these abnormal functions.
authors.affiliation: Neuroendocrine Unit, Multidisciplinary Institute on Cell Biology (CONICET-CICPBA), La Plata, Argentina.
authors.forename: G
authors.initials: G
authors.lastname: Moreno
authors.forename: M
authors.initials: M
authors.lastname: Perelló
authors.forename: G
authors.initials: G
authors.lastname: Camihort
authors.forename: G
authors.initials: G
authors.lastname: Luna
authors.forename: G
authors.initials: G
authors.lastname: Console
authors.forename: R C
authors.initials: RC
authors.lastname: Gaillard
authors.forename: E
authors.initials: E
authors.lastname: Spinedi
mesh_terms: D017667:Adipocytes / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D000273:Adipose Tissue / Q000473:pathology / Q000503:physiopathology; D050154:Adiposity / Q000502:physiology*; D000302:Adrenal Cortex / Q000503:physiopathology*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002478:Cells, Cultured; D003345:Corticosterone / Q000097:blood; D003907:Dexamethasone / Q000494:pharmacology; D005260:Female; D005938:Glucocorticoids / Q000096:biosynthesis; D007027:Hypothalamic Diseases / Q000139:chemically induced / Q000150:complications / Q000503:physiopathology*; D007328:Insulin / Q000097:blood / Q000494:pharmacology; D007333:Insulin Resistance / Q000502:physiology; D020738:Leptin / Q000097:blood; D008297:Male; D009765:Obesity / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012970:Sodium Glutamate
chemical_list: D001786:Blood Glucose; D005938:Glucocorticoids; D007328:Insulin; D020738:Leptin; D003907:Dexamethasone; D012970:Sodium Glutamate; D003345:Corticosterone