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分离的绵羊瘤胃上皮细胞对棕榈酸的代谢

Palmitate metabolism by isolated sheep rumen epithelial cells.

作者信息

Jesse B W, Solomon R K, Baldwin R L

机构信息

Department of Animal Sciences, Rutgers, State University, New Brunswick, NJ 08903.

出版信息

J Anim Sci. 1992 Jul;70(7):2235-42. doi: 10.2527/1992.7072235x.

Abstract

Ruminal palmitate metabolism was examined using an isolated cell system. Palmitate oxidation to 14CO2 by rumen epithelial cells isolated from the rumens of mature sheep was linear during the course of a 2-h incubation (11.1 nmoles.million cells-1.2 h-1) and 3.6 times the rate of palmitate oxidation by cells isolated from neonatal rumen (3.1 nmoles.million cells-1.min-1). Subsequent experiments were conducted with mature rumen epithelial cells. Neither acetate (50 mM), propionate (10 mM), dibutyryl cAMP (.2 mM), nor insulin (10 mU/mL) altered palmitate oxidation to CO2. However, butyrate (10 mM) addition reduced (P less than .05), and ammonia (15 mM) tended to reduce (P less than .10), palmitate oxidation (51.6 and 82.0% of control, respectively), whereas addition of glucose (2.5 mM) increased (P less than .05) palmitate oxidation (151% of control). Of the compounds tested, only propionate, butyrate, and ammonia reduced palmitate oxidation to total acid-soluble metabolites. Propionate (10 mM) addition completely abolished palmitate oxidation to acid-soluble metabolites. Succinate addition (5 to 50 mM) increased palmitate oxidation to CO2 but exhibited no consistent effect on palmitate oxidation to either acid-soluble metabolites or beta-hydroxybutyrate. Propionate completely abolished palmitate oxidation to beta-hydroxybutyrate, suggesting that propionate-induced inhibition of palmitate oxidation is not mediated via succinate. The data indicate 1) that rumen epithelium is capable of oxidizing palmitate, 2) that ruminal palmitate oxidation may be subject to regulation by developmental factors, and 3) that palmitate metabolism seems to be influenced more by ruminally derived metabolites than by factors derived exclusively from the general circulation.

摘要

使用分离细胞系统研究了瘤胃棕榈酸代谢。从成年绵羊瘤胃分离的瘤胃上皮细胞将棕榈酸氧化为(^{14}CO_2)的过程在2小时的孵育过程中呈线性((11.1)纳摩尔·百万细胞(^{-1}\cdot2)小时(^{-1})),是从新生瘤胃分离的细胞棕榈酸氧化速率((3.1)纳摩尔·百万细胞(^{-1}\cdot)分钟(^{-1}))的3.6倍。随后用成年瘤胃上皮细胞进行了实验。乙酸盐((50)毫摩尔)、丙酸盐((10)毫摩尔)、二丁酰环磷腺苷((0.2)毫摩尔)或胰岛素((10)微单位/毫升)均未改变棕榈酸氧化为(CO_2)的过程。然而,添加丁酸盐((10)毫摩尔)会降低((P\lt0.05)),氨((15)毫摩尔)倾向于降低((P\lt0.10))棕榈酸氧化(分别为对照的(51.6%)和(82.0%)),而添加葡萄糖((2.5)毫摩尔)会增加((P\lt0.05))棕榈酸氧化(为对照的(151%))。在所测试的化合物中,只有丙酸盐、丁酸盐和氨降低了棕榈酸氧化为总酸溶性代谢物的过程。添加丙酸盐((10)毫摩尔)完全消除了棕榈酸氧化为酸溶性代谢物的过程。添加琥珀酸盐((5)至(50)毫摩尔)增加了棕榈酸氧化为(CO_2)的过程,但对棕榈酸氧化为酸溶性代谢物或β-羟基丁酸盐没有一致的影响。丙酸盐完全消除了棕榈酸氧化为β-羟基丁酸盐的过程,表明丙酸盐诱导的棕榈酸氧化抑制不是通过琥珀酸盐介导的。数据表明:1)瘤胃上皮能够氧化棕榈酸;2)瘤胃棕榈酸氧化可能受发育因素调节;3)棕榈酸代谢似乎受瘤胃来源的代谢物影响更大,而不是仅来自全身循环的因素。

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