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肉碱在大鼠体内和体外的抗酮血症和抗生酮作用。

Antiketonemic and antiketogenic actions of carnitine in vivo and in vitro in rats.

作者信息

Yeh Y Y

出版信息

J Nutr. 1981 May;111(5):831-40. doi: 10.1093/jn/111.5.831.

DOI:10.1093/jn/111.5.831
PMID:7229733
Abstract

The effect of carnitine on ketone and lipid metabolism in intact rats and in isolated tissues was investigated. DL-Carnitine (200 mg/100 g body weight) administered orally lowered by approximately 40-65% plasma concentrations of ketone bodies in suckling rats and fasted adult rats. It also suppressed hyperketonemia induced by corn oil feeding in suckling and adult rats by approximately 30-60%. Carnitine did not change beta-hydroxybutyrate oxidation in heart and kidney mitochondria. Incubation of carnitine with tissue slices of cerebral cortex, kidney and diaphragm did not affect 14CO2 production or lipid synthesis from DL-[3-14C]-beta-hydroxybutyrate. The compound reduced the urinary concentration and excretion of ketone bodies in rats fed corn oil but had no effect in rats not treated with corn oil. Although DL-carnitine at concentrations ranging from 0.2 to 20 mM stimulated ketone production in hepatocytes, at a higher concentration (i.e., 40 mM) it produced a sharp depression in ketogenesis. These results indicate that carnitine does not stimulate ketone utilization by extrahepatic tissues. The antiketonemic effect of carnitine in rats treated with a high dose of the compound most likely results from inhibition of hepatic ketone production. An excessive increase in free carnitine by exogenous administration could upset the equilibrium fat conversion of acylcarnitine to acylCoA in mitochondria and hence suppress beta-oxidation and ketogenesis.

摘要

研究了肉碱对完整大鼠及离体组织中酮体和脂质代谢的影响。口服给予DL-肉碱(200mg/100g体重)可使乳鼠和禁食成年大鼠血浆中酮体浓度降低约40 - 65%。它还能使乳鼠和成年大鼠因喂食玉米油诱导的高酮血症降低约30 - 60%。肉碱不会改变心脏和肾脏线粒体中β-羟基丁酸的氧化。将肉碱与大脑皮层、肾脏和膈肌的组织切片一起孵育,不会影响DL-[3-14C]-β-羟基丁酸的14CO2生成或脂质合成。该化合物可降低喂食玉米油的大鼠尿液中酮体的浓度和排泄量,但对未用玉米油处理的大鼠没有影响。尽管浓度在0.2至20mM范围内的DL-肉碱可刺激肝细胞产生酮体,但在较高浓度(即40mM)时,它会使酮体生成急剧降低。这些结果表明,肉碱不会刺激肝外组织利用酮体。肉碱对高剂量该化合物处理的大鼠的抗酮血症作用很可能是由于抑制了肝脏中酮体的生成。外源性给予导致游离肉碱过度增加,可能会破坏线粒体中酰基肉碱向酰基辅酶A的脂肪转化平衡,从而抑制β-氧化和酮体生成。

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J Nutr. 1981 May;111(5):831-40. doi: 10.1093/jn/111.5.831.
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