Jesse B W, Emery R S, Thomas J W
J Dairy Sci. 1986 Sep;69(9):2290-7. doi: 10.3168/jds.S0022-0302(86)80667-1.
Fatty acid oxidation by bovine liver slices and mitochondria was examined to determine potential regulatory sites of fatty acid oxidation. Conversion of 1-[14C]palmitate to 14CO2 and total [14C]acid-soluble metabolites was used to measure fatty acid oxidation. Oxidation of palmitate (1 mM) was linear in both liver slice weight and incubation time. Carnitine stimulated palmitate oxidation; 2 mM dl-carnitine produced maximal stimulation of palmitate oxidation to both CO2 and acid-soluble metabolites. Propionate (10 mM) inhibited palmitate oxidation by bovine liver slices. Clofenapate, an inhibitor of fatty acid esterification, alone increased palmitate oxidation and was able to prevent the propionate-induced inhibition of palmitate oxidation by liver slices. Propionate (.5 to 10 mM) had no effect on palmitate oxidation by mitochondria, but malonyl Coenzyme A, the first committed intermediate of fatty acid synthesis, inhibited mitochondrial palmitate oxidation (inhibition constant = .3 microM). Liver mitochondrial carnitine palmitoyltransferase (EC 2.3.1.21) exhibited Michaelis constants for palmitoyl Coenzyme A and l-carnitine of 11.5 microM and .59 mM, respectively. Long-chain fatty acid oxidation in bovine liver is regulated by mechanisms similar to those in rats but adapted to the unique digestive physiology of the bovine.
通过检测牛肝切片和线粒体的脂肪酸氧化，以确定脂肪酸氧化的潜在调控位点。利用1-[14C]棕榈酸酯转化为14CO2以及总的[14C]酸溶性代谢产物来测量脂肪酸氧化。棕榈酸酯（1 mM）的氧化在肝切片重量和孵育时间方面均呈线性。肉碱刺激棕榈酸酯氧化；2 mM的dl-肉碱对棕榈酸酯氧化为CO2和酸溶性代谢产物产生最大刺激作用。丙酸盐（10 mM）抑制牛肝切片的棕榈酸酯氧化。氯苯那酯，一种脂肪酸酯化抑制剂，单独使用时可增加棕榈酸酯氧化，并能够防止丙酸盐诱导的肝切片对棕榈酸酯氧化的抑制作用。丙酸盐（0.5至10 mM）对线粒体的棕榈酸酯氧化没有影响，但丙二酰辅酶A，脂肪酸合成的第一个关键中间产物，抑制线粒体棕榈酸酯氧化（抑制常数 = 0.3 microM）。肝线粒体肉碱棕榈酰转移酶（EC 2.3.1.21）对棕榈酰辅酶A和l-肉碱的米氏常数分别为11.5 microM和0.59 mM。牛肝中的长链脂肪酸氧化受与大鼠相似的机制调控，但适应了牛独特的消化生理学特点。
