title: Glucocorticoid-dependency of increased adiposity in a model of hypothalamic obesity.
abstract: It is known that rats treated, at neonatal age, with monosodium L-glutamate (MSG) develop neuroendocrine and metabolic abnormalities, resulting in a phenotype of hypothalamic obesity, characterized by increased adiposity, corticosteronemia and leptinemia.
  
  
  OBJECTIVE
  We explored whether adrenal manipulations could result in the reversion of this phenotype of hypothalamic obesity.
  
  
  METHODS
  Newborn male rats, treated with MSG or vehicle (CTR), were submitted to sham operation, bilateral adrenalectomy (ADX) or bilateral adrenal enucleation (AE) on day 120 of age. Animals were examined 21 days after ADX, combined or not with corticosterone (B) substitution (ADX+B), and on days 21 and 35 after AE. Food intake, body weight and body fat mass were monitored; additionally circulating levels of insulin, leptin, ACTH and B were measured.
  
  
  RESULTS
  Our data indicate that: a) normalization of basal B circulating levels in, 21 day-ADX and -AE, MSG rats fully reversed hyperinsulinemia, hyperleptinemia and significantly decreased body fat mass; and b) recovery of hypercorticosteronemia in, 35 day-AE, MSG rats fully restored this phenotype of hypothalamic obesity.
  
  
  CONCLUSIONS
  Our study strongly supports that high glucocorticoid production is the main factor responsible for the development of enhanced adiposity in MSG rats and, importantly, that this abnormality could be reversed by an appropriate therapy.
authors.affiliation: Neuroendocrine Unit, Multidisciplinary Institute on Cell Biology (CONICET-CICPBA), 1900 La Plata, Argentina.
authors.forename: Mario
authors.initials: M
authors.lastname: Perelló
authors.forename: Griselda
authors.initials: G
authors.lastname: Moreno
authors.forename: Rolf C
authors.initials: RC
authors.lastname: Gaillard
authors.forename: Eduardo
authors.initials: E
authors.lastname: Spinedi
mesh_terms: D000273:Adipose Tissue / Q000502:physiology; D000311:Adrenal Glands / Q000502:physiology*; D000315:Adrenalectomy; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D000831:Animals, Newborn; D001111:Arcuate Nucleus of Hypothalamus / Q000187:drug effects / Q000503:physiopathology*; D001823:Body Composition / Q000502:physiology; D003345:Corticosterone / Q000097:blood / Q000502:physiology*; D004435:Eating / Q000502:physiology; D005260:Female; D007031:Hypothalamus / Q000187:drug effects / Q000503:physiopathology; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood*; D008297:Male; D009765:Obesity / Q000097:blood* / Q000139:chemically induced / Q000517:prevention & control; D051381:Rats; D017207:Rats, Sprague-Dawley; D012970:Sodium Glutamate
chemical_list: D007328:Insulin; D020738:Leptin; D000324:Adrenocorticotropic Hormone; D012970:Sodium Glutamate; D003345:Corticosterone