Orellana M, Fuentes O, Valdés E
Departamento de Bioquimica, Facultad de Medicina, Universidad de Chile, Santiago.
FEBS Lett. 1993 May 3;322(1):61-4. doi: 10.1016/0014-5793(93)81111-c.
Microsomal lauric acid 12-hydroxy lauric acid (omega)-hydroxylation and fatty acid peroxisomal beta-oxidation were studied in kidney tissue from starved rats. Starvation increased the microsomal omega-hydroxylation and peroxisomal beta-oxidation of fatty acids with a high correlation between both processes. Earlier, we reported similar results in liver. Our results support the hypothesis that the role of microsomal fatty acids omega-hydroxylation is the generation of substrate for peroxisomal beta-oxidation, with the final purpose of contributing to a catabolic or gluconeogenic pathway from fatty acids.
在饥饿大鼠的肾脏组织中研究了微粒体月桂酸12-羟基月桂酸(ω)-羟基化和脂肪酸过氧化物酶体β-氧化。饥饿增加了微粒体ω-羟基化和脂肪酸过氧化物酶体β-氧化,且这两个过程之间具有高度相关性。此前,我们在肝脏中也报道过类似结果。我们的结果支持这样的假说,即微粒体脂肪酸ω-羟基化的作用是为过氧化物酶体β-氧化生成底物,最终目的是促进脂肪酸的分解代谢或糖异生途径。