title: A palatable hyperlipidic diet causes obesity and affects brain glucose metabolism in rats.
abstract: BACKGROUND
  We have previously shown that either the continuous intake of a palatable hyperlipidic diet (H) or the alternation of chow (C) and an H diet (CH regimen) induced obesity in rats. Here, we investigated whether the time of the start and duration of these feeding regimens are relevant and whether they affect brain glucose metabolism.
  
  
  METHODS
  Male Wistar rats received C, H, or CH diets during various periods of their life spans: days 30-60, days 30-90, or days 60-90. Experiments were performed the 60th or the 90th day of life. Rats were killed by decapitation. The glucose, insulin, leptin plasma concentration, and lipid content of the carcasses were determined. The brain was sliced and incubated with or without insulin for the analysis of glucose uptake, oxidation, and the conversion of [1-14C]-glucose to lipids.
  
  
  RESULTS
  The relative carcass lipid content increased in all of the H and CH groups, and the H30-60 and H30-90 groups had the highest levels. Groups H30-60, H30-90, CH30-60, and CH30-90 exhibited a higher serum glucose level. Serum leptin increased in all H groups and in the CH60-90 and CH30-90 groups. Serum insulin was elevated in the H30-60, H60-90, CH60-90, CH30-90 groups. Basal brain glucose consumption and hypothalamic insulin receptor density were lower only in the CH30-60 group. The rate of brain lipogenesis was increased in the H30-90 and CH30-90 groups.
  
  
  CONCLUSIONS
  These findings indicate that both H and CH diet regimens increased body adiposity independent treatment and the age at which treatment was started, whereas these diets caused hyperglycemia and affected brain metabolism when started at an early age.
authors.affiliation: Disciplina de Fisiologia da Nutrição, Departamento de Fisiologia, Universidade Federal de São Paulo, São Paulo, SP, Brazil.
authors.forename: Debora
authors.initials: D
authors.lastname: Estadella
authors.forename: Lila M
authors.initials: LM
authors.lastname: Oyama
authors.forename: Allain A
authors.initials: AA
authors.lastname: Bueno
authors.forename: Carlos A
authors.initials: CA
authors.lastname: Habitante
authors.forename: Gabriel I
authors.initials: GI
authors.lastname: Souza
authors.forename: Eliane B
authors.initials: EB
authors.lastname: Ribeiro
authors.forename: Caio S M
authors.initials: CS
authors.lastname: Motoyama
authors.forename: Claudia M
authors.initials: CM
authors.lastname: Oller do Nascimento
mesh_terms: D000375:Aging / Q000097:blood / Q000378:metabolism; D000818:Animals; D001522:Behavior, Animal; D001921:Brain / Q000378:metabolism*; D004036:Diet, Atherogenic / Q000009:adverse effects*; D002149:Energy Intake; D005247:Feeding Behavior; D005947:Glucose / Q000378:metabolism*; D006019:Glycolysis; D006943:Hyperglycemia / Q000209:etiology; D007031:Hypothalamus / Q000378:metabolism; D007328:Insulin / Q000097:blood / Q000378:metabolism; D020738:Leptin / Q000097:blood; D050155:Lipogenesis; D008297:Male; D009419:Nerve Tissue Proteins / Q000378:metabolism; D009474:Neurons / Q000378:metabolism; D009765:Obesity / Q000097:blood / Q000209:etiology* / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D011972:Receptor, Insulin / Q000378:metabolism; D054411:Receptors, Leptin / Q000378:metabolism
chemical_list: D007328:Insulin; D020738:Leptin; D009419:Nerve Tissue Proteins; D054411:Receptors, Leptin; D011972:Receptor, Insulin; D005947:Glucose