title: Perinatal overfeeding in rats results in increased levels of plasma leptin but unchanged cerebrospinal leptin in adulthood.
abstract: OBJECTIVE
  To study the effect of perinatal programming and overfeeding on the hypothalamic control mechanisms of food intake in adult rats.
  
  
  METHODS
  Neonatal programming effects on body weight, food intake, central and peripheral leptin levels, hypothalamic neuropeptides, leptin receptors and central leptin responsiveness in adult rats.
  
  
  METHODS
  Plasma and cerebrospinal fluid (CSF) leptin levels were analyzed using radioimmunoassay. Neuropeptide mRNA levels were analyzed using in situ hybridization. Leptin receptor mRNA levels were analyzed using reverse transcriptase-polymerase chain reaction.
  
  
  RESULTS
  Perinatally overfed rats growing up in small litters (SL) maintain their obese and hyperleptinemic phenotype in adulthood. However, leptin levels in CSF are abnormally low considering the plasmatic hyperleptinemia. In contrast to the already reported changes in perinatally overfed juvenile rats, perinatally overfed adult rats did not show any alteration in the expression of leptin receptor isoforms and evaluated neuropeptides. Moreover, SL adult rats showed a normal sensitivity regarding the inhibitory effect of intracerebroventricular leptin administration on food intake.
  
  
  CONCLUSIONS
  Perinatal overfeeding does not induce alterations in either the anorectic response to central leptin administration or expression of leptin receptors and neuropeptides in adulthood. The leptin resistance to peripheral leptin in SL adult rats may be related to impaired leptin transport across the blood-brain barrier.
authors.affiliation: Department of Physiology, School of Medicine, University of Santiago de Compostela, S Francisco s/n, Santiago de Compostela (A Coruña), Spain.
authors.forename: M
authors.initials: M
authors.lastname: López
authors.forename: S
authors.initials: S
authors.lastname: Tovar
authors.forename: M J
authors.initials: MJ
authors.lastname: Vázquez
authors.forename: R
authors.initials: R
authors.lastname: Nogueiras
authors.forename: L M
authors.initials: LM
authors.lastname: Seoane
authors.forename: M
authors.initials: M
authors.lastname: García
authors.forename: R M
authors.initials: RM
authors.lastname: Señarís
authors.forename: C
authors.initials: C
authors.lastname: Diéguez
mesh_terms: D000818:Animals; D001812:Blood-Brain Barrier / Q000502:physiology; D049628:Body Size / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D004435:Eating / Q000187:drug effects / Q000502:physiology*; D005260:Female; D005786:Gene Expression Regulation; D007031:Hypothalamus / Q000378:metabolism; D017403:In Situ Hybridization; D020738:Leptin / Q000097:blood* / Q000134:cerebrospinal fluid / Q000494:pharmacology; D009479:Neuropeptides / Q000096:biosynthesis / Q000235:genetics; D009765:Obesity / Q000097:blood / Q000134:cerebrospinal fluid / Q000503:physiopathology; D011247:Pregnancy; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D011956:Receptors, Cell Surface / Q000096:biosynthesis / Q000235:genetics; D054411:Receptors, Leptin; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods
chemical_list: D020738:Leptin; D009479:Neuropeptides; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin