RELATIONSHIP BETWEEN ACID-SOLUBLE CARNITINE AND COENZYME-A POOLS INVIVO

RELATIONSHIP BETWEEN ACID-SOLUBLE CARNITINE AND COENZYME-A POOLS INVIVO
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DOI:
10.1042/bj1900495
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发表时间:
1980-01-01
影响因子:
4.1
通讯作者:
HOPPEL, CL
HOPPEL, CL
中科院分区:
生物学3区
文献类型:
--
作者:
BRASS, EP;HOPPEL, CL

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在进食和24 h饥饿大鼠中研究了给予肉毒碱后酸溶性肉毒碱和辅酶A库之间的关系。以60 μ mol/100 g体重的剂量通过静脉注射给予的肉毒碱被整合到动物的内源性肉毒碱库中。在注射肉毒碱后5 min内,血浆和肝脏中出现大量的酰基肉毒碱。注射后观察到进食和饥饿大鼠之间酸溶性酰基肉毒碱浓度的差异,反映了2种代谢状态的内源性肉毒碱库中所见的酰基肉毒碱/肉毒碱关系。一个更大的酰基肉毒碱生产中看到饥饿的动物,并表示更大的来源,可访问的酰基辅酶A分子。除了存在的酰基肉毒碱的量的变化之外,存在的特定酰基也在动物组之间变化。乙酰肉毒碱组成的37和53%的肝酸溶性酰基肉毒碱在未注射喂养和饥饿的动物,分别。在5分钟后,肉毒碱注射肝酸溶性酰基肉毒碱分别为41%和73%的乙酰肉毒碱的形式在喂养和饥饿大鼠,分别。尽管肉毒碱和酰基肉毒碱有这些大的变化,但在血浆非酯化脂肪酸或β-脂肪酸中没有观察到变化。在喂食或饥饿的大鼠中的羟基丁酸盐浓度。乙酰辅酶A,辅酶A,总酸溶性辅酶A和酸不溶性辅酶A的测量表明,肝脏辅酶A池是抵抗肉毒碱诱导的变化。这种缺乏变化的肝脏CoA池或酮体的生产,而酰基从酰基辅酶A分子分流到酰基肉毒碱表明通过肉毒碱池与CoA池相比,流量低。肉毒碱/酸溶性酰基肉毒碱库明显反映了肝脏CoA/酰基CoA库的变化,而不是诱导变化。
The relationship between the acid-soluble carnitine and coenzyme A pools was studied in fed and 24 h starved rats after carnitine administration. Carnitine given by i.v. injection at a dose of 60 .mu.mol/100 g body wt was integrated into the animal''s endogenous carnitine pool. Large amounts of acylcarnitines appeared in the plasma and liver within 5 min of carnitine injection. Differences in acid-soluble acylcarnitine concentrations were observed between fed and starved rats after injection and reflected the acylcarnitine/carnitine relationship seen in the endogenous carnitine pool of the 2 metabolic states. A larger acylcarnitine production was seen in starved animals and indicated a greater source of accessible acyl-CoA molecules. In addition to changes in the amount of acylcarnitines present, the specific acyl groups present also varied between groups of animals. Acetylcarnitine made up 37 and 53% of liver acid-soluble acylcarnitines in uninjected fed and starved animals, respectively. At 5 min after carnitine injection hepatic acid-soluble acylcarnitines were 41 and 73% in the form of acetylcarnitine in fed and starved rats, respectively. Despite these large changes in carnitine and acylcarnitines, no changes were observed in plasma non-esterified fatty acid or .beta.-hydroxybutyrate concentrations in either fed or starved rats. Measurement of acetyl-CoA, CoA, total acid-soluble CoA and acid-insoluble CoA demonstrated that the hepatic CoA pool was resistant to carnitine-induced changes. This lack of change in the hepatic CoA pool or ketone-body production while acyl groups are shunted from acyl-CoA molecules to acylcarnitines suggests a low flux through the carnitine pool compared with the CoA pool. The carnitine/acid-soluble acylcarnitine pool apparently reflects changes in, rather than inducing changes in, the hepatic CoA/acyl-CoA pool.