RESUMO
Dietary sphingolipids (SL) inhibit colon carcinogenesis, reduce serum cholesterol, and improve skin barrier function and are considered to be "functional lipids". For comparative determination of the effects of SL with different chemical compositions on lipid metabolism and its related hepatic gene expression, Zucker fatty rats were fed pure sphingomyelin (SM) of animal origin and glucosylceramide (GC) of plant origin. After 45 days, the SM and GC diets led to significant reductions in hepatic lipid and plasma non-HDL cholesterol. Both SM and GC diets decreased plasma insulin levels, whereas only the GC diet increased the plasma adiponectin level. Hepatic gene expression analysis revealed increased expression of adiponectin receptor 2 (Adipor2), peroxisome proliferator-activated receptor alpha (PPARalpha), and pyruvate dehydrogenase kinase 4 (Pdk4). However, expression of stearoyl CoA desaturase (Scd1) was significantly decreased. These results suggest that dietary SL, even of different origins and chemical compositions, may prevent fatty liver and hypercholesterolemia through improvement of adiponectin signaling and consequent increases in insulin sensitivity.
Assuntos
Glucosilceramidas/administração & dosagem , Hiperlipidemias/tratamento farmacológico , Hiperlipidemias/metabolismo , Metabolismo dos Lipídeos/efeitos dos fármacos , Esfingomielinas/administração & dosagem , Animais , Modelos Animais de Doenças , Expressão Gênica/efeitos dos fármacos , Humanos , Hiperlipidemias/genética , Insulina/sangue , Fígado/efeitos dos fármacos , Fígado/metabolismo , Masculino , Ratos , Ratos Zucker , Receptores de Adiponectina/genética , Receptores de Adiponectina/metabolismoRESUMO
To identify novel functions of the oral intake of sweet corn, we performed DNA microarray analysis of the livers of sweet corn-fed mice. Functional annotation clustering 1600 genes with expression levels that were affected (more than 1.5-fold change) by dietary sweet corn indicated that both cell proliferation and programmed cell death were modulated by sweet corn intake. In the Wnt signaling pathway, which is involved in cell proliferation, the levels of Jun and beta-catenin expression were downregulated by dietary sweet corn. The mRNA levels of Rb and p53, negative regulators of the cell cycle, were increased in mice fed with sweet corn. Dietary corn upregulated expression levels of genes that regulate apoptosis positively (for example, BOK, BID, CASP4). These results suggested that sweet corn is a valuable food for suppressing cancer. Oral administration of sweet corn inhibited tumor growth (36.6% reduce in tumor weight, P < 0.05) in mice inoculated with Ehrlich tumor cells.