McGarry J D, Robles-Valdes C, Foster D W
Proc Natl Acad Sci U S A. 1975 Nov;72(11):4385-8. doi: 10.1073/pnas.72.11.4385.
The enhancement of long-chain fatty acid oxidation and ketogenesis in the perfused rat liver, whether induced acutely by treatment of fed animals with anti-insulin serum or glucagon, or over the longer term by starvation or the induction of alloxan diabetes, was found to ba accompanied by a proportional elevation in the tissue carnitine content. Moreover, when added to the medium perfusing livers from fed rats, carnitine stimulated ketogenesis from oleic acid. The findings suggest that the increased fatty acid flux through the carnitine acyltransferase (carnitine palmitoyl-transferase; palmitoyl-CoA:L-carnitine O-palmitoyltransferase; EC 2.3.1.21) reaction brought about by glucagon excess, with or without insulin deficiency, is mediated, at least in part, by elevation in the liver carnitine concentration.
无论是通过用抗胰岛素血清或胰高血糖素急性处理喂食的动物,还是通过长期饥饿或诱导四氧嘧啶糖尿病,灌注大鼠肝脏中长链脂肪酸氧化和生酮作用的增强,都伴随着组织肉碱含量的相应升高。此外,当将肉碱添加到灌注喂食大鼠肝脏的培养基中时,它会刺激油酸的生酮作用。这些发现表明,由胰高血糖素过量引起的、无论有无胰岛素缺乏的情况下,通过肉碱酰基转移酶(肉碱棕榈酰转移酶;棕榈酰辅酶A:L-肉碱O-棕榈酰转移酶;EC 2.3.1.21)反应的脂肪酸通量增加,至少部分是由肝脏肉碱浓度升高介导的。