title: Prolonged but not short negative energy condition restored corticoadrenal leptin sensitivity in the hypothalamic obese rat.
abstract: OBJECTIVE
  We have reported that neonatal treatment with monosodium L-glutamate (MSG), which causes damage to the arcuate nucleus, leads to severe hyperleptinemia and reduced adrenal leptin receptor (ob-Rb) expression in adulthood. As a result, rats given MSG neonatally display corticoadrenal leptin-resistance, a defect that is overridden by normalization of corticoadrenal hyperfunction. The aim of the present study was to determine whether negative energy conditions could correct corticoadrenal cell dysfunction in rats given MSG neonatally.
  
  
  METHODS
  Normal (CTR) and MSG-treated female rats were subjected to food removal for 1-5 days, or prolonged (24-61 days) food restriction (FR). Plasma levels of several biomarkers and in vitro corticoadrenal function were evaluated following starvation or FR.
  
  
  RESULTS
  Fasting for 1-5 days reduced plasma leptin levels in CTR and MSG rats, compared to levels in the respective groups fed ad libitum(p < 0.05), but adrenal leptin-resistance was unchanged. With prolonged FR, isolated adrenal cells from MSG rats became sensitive to leptin, which lowered ACTH-induced glucocorticoid release. This restoration of leptin response was associated with normalization of adrenal ob-Rb gene expression.
  
  
  CONCLUSIONS
  Dietary restriction in some leptin-resistant obese phenotypes may normalize adrenocortical function.
authors.affiliation: Neuroendocrine Unit, Multidisciplinary Institute on Cell Biology (CONICET-CICPBA), La Plata, Argentina.
authors.forename: Mario
authors.initials: M
authors.lastname: Perello
authors.forename: Daniel
authors.initials: D
authors.lastname: Castrogiovanni
authors.forename: Andrés
authors.initials: A
authors.lastname: Giovambattista
authors.forename: Rolf C
authors.initials: RC
authors.lastname: Gaillard
authors.forename: Eduardo
authors.initials: E
authors.lastname: Spinedi
mesh_terms: D000302:Adrenal Cortex / Q000187:drug effects* / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000097:blood / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D001798:Blood Proteins; D001835:Body Weight; D003345:Corticosterone / Q000378:metabolism; D002149:Energy Intake / Q000502:physiology*; D005260:Female; D005508:Food Deprivation / Q000502:physiology; D007031:Hypothalamus / Q000378:metabolism*; D020738:Leptin / Q000097:blood* / Q000494:pharmacology; D008297:Male; D009765:Obesity / Q000378:metabolism*; D009929:Organ Size; D011247:Pregnancy; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D054411:Receptors, Leptin / Q000235:genetics; D012970:Sodium Glutamate / Q000494:pharmacology*; D013997:Time Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D001798:Blood Proteins; D020738:Leptin; D012333:RNA, Messenger; D054411:Receptors, Leptin; D014280:Triglycerides; D000324:Adrenocorticotropic Hormone; D012970:Sodium Glutamate; D003345:Corticosterone