title: Down-regulation of CCAAT/enhancer binding proteins alpha, beta and delta in adipose tissue by intracerebroventricular leptin in rats.
abstract: In our previous report, intracerebroventricular (i.c.v.) administration of leptin caused fat depletion by an induced adipocyte apoptosis in addition to influencing lipid metabolism. To uncover the biochemical mechanisms that mediate this response, the present study was designed to determine whether CCAAT/enhancer binding proteins (C/EBP)alpha, -beta and -delta play a role in the leptin-induced fat depletion. Expressions of C/EBPalpha, -beta and -delta in epididymal fat tissues were examined by Western immunoblot and in situ immunocytochemical analysis after 5 days of i.c.v. treatment. Young and old rats (3 and 8 months old) were treated with or without 5 micrograms/day leptin. The expression of C/EBPalpha, -beta and -delta was decreased by i.c.v. leptin treatment in young rats as compared with controls (P<0.05). However, leptin did not influence the expression of C/EBPalpha, -beta and -delta in adipose tissues of 8-month-old rats. The basal level of expression of C/EBPbeta was greater in 8-month-old rats than in 3-month-old rats, (P<0.05) whereas the basal expression of C/EBPalpha and -delta was not different between age groups. These results were confirmed by in situ immunocytochemical analysis. The present study suggests that leptin-induced down-regulation of C/EBPalpha, -beta and -delta might influence adipocyte differentiation and growth in a number of ways.
authors.affiliation: Department of Foods and Nutrition, The University of Georgia, Athens, GA 30602, USA.
authors.forename: H
authors.initials: H
authors.lastname: Qian
authors.forename: G J
authors.initials: GJ
authors.lastname: Hausman
authors.forename: M M
authors.initials: MM
authors.lastname: Compton
authors.forename: M J
authors.initials: MJ
authors.lastname: Azain
authors.forename: D L
authors.initials: DL
authors.lastname: Hartzell
authors.forename: C A
authors.initials: CA
authors.lastname: Baile
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism*; D000375:Aging; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D022762:CCAAT-Enhancer-Binding Proteins; D002552:Cerebral Ventricles / Q000187:drug effects / Q000502:physiology*; D004268:DNA-Binding Proteins / Q000096:biosynthesis / Q000235:genetics*; D002149:Energy Intake / Q000187:drug effects; D004742:Enhancer Elements, Genetic; D004822:Epididymis; D004926:Escherichia coli; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects; D007150:Immunohistochemistry; D007276:Injections, Intraventricular; D020738:Leptin; D008297:Male; D009687:Nuclear Proteins / Q000096:biosynthesis / Q000235:genetics*; D011506:Proteins / Q000008:administration & dosage / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011994:Recombinant Proteins / Q000008:administration & dosage / Q000494:pharmacology
chemical_list: D022762:CCAAT-Enhancer-Binding Proteins; D004268:DNA-Binding Proteins; D020738:Leptin; D009687:Nuclear Proteins; D011506:Proteins; D011994:Recombinant Proteins