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Br J Nutr ; 89(3): 429-38, 2003 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-12628037

RESUMO

The present study was designed to define how dietary fat type regulates body adiposity in dietary obesity-susceptible (DOS) Sprague-Dawley (SD) rats. Eighty-three SD rats received a purified diet containing 50 g maize oil (MO)/kg for 3 weeks and then thirty-nine of the rats, designated as the DOS rats, were allotted to diets containing 160 g MO (DOS-MO), beef tallow (DOS-BT) or fish oil (DOS-FO)/kg for 9 weeks. As a result of the experiment, the DOS-FO rats had significantly (P<0.05) reduced weight gain and abdominal and epididymal fat-pad mass than the DOS-MO and DOS-BT rats. Serum leptin level was also significantly (P<0.05) lower in the DOS-FO rats; however, hypothalamic leptin receptor (a and b) mRNA and neuropeptide Y expressions were not altered by dietary fat sources. A lower acetyl-CoA carboxylase mRNA expression in the liver was observed in the DOS-FO group, whereas hepatic peroxisome proliferator-activated receptor-gamma mRNA and protein expressions were markedly elevated in the DOS-FO group compared with those in the other groups. We did not observe differences in acetyl-CoA carboxylase and peroxisome proliferator-activated receptor-gamma expressions in epididymal fat of the DOS rats consuming MO, BT or FO. It is concluded from our present observations that dietary fat type, especially that rich in FO, plays a potential role in down-regulation of adiposity by altering hepatic lipogenic genes, rather than feeding behaviour, in the DOS-SD rats.


Assuntos
Tecido Adiposo/efeitos dos fármacos , Gorduras na Dieta/farmacologia , Suscetibilidade a Doenças , Obesidade/etiologia , Acetil-CoA Carboxilase/metabolismo , Animais , Bovinos , Óleo de Milho/farmacologia , Ingestão de Alimentos , Óleos de Peixe/farmacologia , Regulação da Expressão Gênica/efeitos dos fármacos , Leptina/sangue , Fígado/metabolismo , Masculino , Neuropeptídeo Y/metabolismo , Ratos , Ratos Sprague-Dawley , Receptores de Superfície Celular/metabolismo , Receptores Citoplasmáticos e Nucleares/metabolismo , Receptores para Leptina , Fatores de Transcrição/metabolismo , Aumento de Peso/efeitos dos fármacos
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