Departamento de Fisiología de la Nutrición, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico, DF, Mexico.
J Nutr. 2013 Aug;143(8):1211-8. doi: 10.3945/jn.113.176354. Epub 2013 Jun 12.
Body nitrogen retention is dependent on the amount of dietary protein consumed, as well as the fat and carbohydrate content in the diet, due to the modulation of amino acid oxidation. PPARα is a transcription factor involved in the upregulation of the expression of enzymes of fatty acid oxidation. However, the role of putative PPARα response elements (PPREs) in the promoter of several amino acid-degrading enzymes (AADEs) is not known. The aim of this work was to study the effect of the synthetic ligand Wy 14643 and the natural ligands palmitate, oleate, and linoleate in rats fed graded concentrations of dietary protein (6, 20, or 50 g/100 g of total diet) on the expression of the AADEs histidase, serine dehydratase, and tyrosine aminotransferase. Thus, we fed male Wistar rats diets containing 6, 20, or 50% casein for 10 d. The results showed that addition of Wy 14643 to the diet significantly reduced the expression of the AADEs. Furthermore, the incubation of hepatocytes with natural ligands of PPARα or feeding rats with diets containing soybean oil, safflower oil, lard, or coconut oil as sources of dietary fat significantly repressed the expression of the AADEs. Gene reporter assays and mobility shift assays demonstrated that the PPRE located at -482 bp of the histidase gene actively bound PPARα in rat hepatocytes. These data indicate that PPARα ligands may reduce amino acid catabolism in rats.
体氮潴留取决于饮食中蛋白质的摄入量，以及饮食中的脂肪和碳水化合物含量，因为这会调节氨基酸的氧化。过氧化物酶体增殖物激活受体α（PPARα）是一种转录因子，参与上调脂肪酸氧化酶的表达。然而，在几种氨基酸降解酶（AADEs）的启动子中，假定的 PPARα 反应元件（PPREs）的作用尚不清楚。本研究的目的是研究在不同蛋白质摄入量（6、20 或 50 g/100 g 总饮食）的大鼠中，合成配体 Wy 14643 和天然配体棕榈酸、油酸和亚油酸对 AADEs 组氨酸酶、丝氨酸脱水酶和酪氨酸转氨酶表达的影响。因此，我们用含有 6、20 或 50%酪蛋白的饮食喂养雄性 Wistar 大鼠 10 天。结果表明，饮食中添加 Wy 14643 可显著降低 AADEs 的表达。此外，用天然的 PPARα 配体孵育肝细胞或用大豆油、红花油、猪油或椰子油作为饮食脂肪来源喂养大鼠，均可显著抑制 AADEs 的表达。基因报告基因检测和电泳迁移率变动分析表明，组氨酸酶基因的-482 bp 处的 PPRE 可在大鼠肝细胞中与 PPARα 结合。这些数据表明，PPARα 配体可能会降低大鼠的氨基酸代谢。
