REGULATION OF GLUCOSE UPTAKE BY MUSCLE .8. EFFECTS OF FATTY ACIDS KETONE BODIES + PYRUVATE + OF ALLOXANDIABETES + STARVATION ON UPTAKE + METABOLIC FATE OF GLUCOSE IN RAT HEART + DIAPHRAGM MUSCLES
REGULATION OF GLUCOSE UPTAKE BY MUSCLE .8. EFFECTS OF FATTY ACIDS KETONE BODIES + PYRUVATE + OF ALLOXANDIABETES + STARVATION ON UPTAKE + METABOLIC FATE OF GLUCOSE IN RAT HEART + DIAPHRAGM MUSCLES
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DOI：
10.1042/bj0930652
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发表时间：
1964-01-01
影响因子：
4.1
通讯作者：
NEWSHOLME, EA
中科院分区：
文献类型：
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作者：
RANDLE, PJ;GARLAND, PB;NEWSHOLME, EA
本文比较了脂肪酸和酮体对大鼠心脏和膈肌葡萄糖摄取和代谢的影响，并与四氧嘧啶糖尿病和饥饿引起的结果进行了比较。戊糖L-阿拉伯糖的膜转运率是更大的心脏从喂养的大鼠比在心脏从大鼠饥饿18 hr. This差异是由于较高的血浆浓度的胰岛素（加速运输的戊糖）在喂养的大鼠。DL-[β]-羟基丁酸酯和正辛酸酯抑制进食大鼠心脏中的L-阿拉伯糖转运。在饥饿大鼠的心脏运输不抑制这些底物，除非胰岛素是在一个低浓度（0.5毫单位/毫升）。在高浓度胰岛素（0.1单位/ml）下，这些底物不抑制转运。有人建议，这些基板可能会损害对胰岛素刺激的运输系统的敏感性。这些底物对葡萄糖转运的类似抑制作用的证据。在用含有葡萄糖（1 mg/ml）和胰岛素（0.1单位/ml）的培养基灌注的正常喂养大鼠心脏中，通过向灌注培养基中添加乙酰乙酸、DL-[β]-羟基丁酸、丁酸、正辛酸、丙酮酸、棕榈酸和油酸（最后2种作为与2%牛血浆白蛋白的复合物）诱导葡萄糖摄取和葡萄糖细胞内蓄积的抑制。结果表明，这些底物对大鼠心脏葡萄糖磷酸化有抑制作用。这些底物对葡萄糖磷酸化的影响与之前在糖尿病或饥饿大鼠心脏中证明的影响相似。这些底物对葡萄糖磷酸化的影响，如糖尿病或饥饿，被水杨酸盐和缺氧所消除。当灌流的大鼠心脏中的葡萄糖摄取被脂肪酸、去音调体或丙酮酸盐抑制时，糖酵解的速率显著降低，而糖原的净合成要么不变要么增加。丁酸盐和棕榈酸盐（由0.85%牛血浆白蛋白携带）对大鼠半横膈葡萄糖摄取和代谢的类似作用已得到证实。在灌流的大鼠心脏中，[1-C14]葡萄糖的C14 O2输出量大于[6-C14]葡萄糖的C14 O2输出量，由此推断，在该组织中，部分葡萄糖通过磷酸戊糖途径被氧化。的可能性，脂肪酸释放在体外从糖尿病大鼠肌肉中的肌肉甘油酯是负责受损的葡萄糖转运，葡萄糖磷酸化，糖酵解，果糖6-磷酸磷酸化和丙酮酸脱氢酶的丙酮酸氧化率的证据进行了总结和讨论。
The effects of fatty acids and ketone bodies on the uptake and metabolic fate of glucose in rat heart and rat diaphragm were compared with those induced by alloxan-diabetes and starvation. The rate of membrane transport of the pentose L-arabinose was greater in hearts from fed rats than in hearts from rats starved for 18 hr. This difference was attributed to the higher plasma concentration of insulin (which accelerates transport of the pentose) in fed rats. DL-[beta]-Hydroxybutyrate and n-octanoate inhibited L-arabinose transport in hearts from fed rats. In hearts from starved rats transport was not inhibited by these substrates unless insulin was present at a low concentration (0.5 milliunit/ml). At high concentrations of insulin (0.1 unit/ml) these substrates did not inhibit transport. It is suggested that these substrates may impair the sensitivity of the transport system towards stimulation by insulin. Evidence is presented for a similar inhibitory effect of these substrates on glucose transport. In hearts from normal fed rats perfused with medium containing glucose (1 mg/ml) and insulin (0.1 unit/ml) inhibition of glucose uptake and intracellular accumulation of glucose was induced by the addition to the perfusion medium of acetoacetate, DL-[beta]-hydroxybutyrate, butyrate, n-octanoate, pyruvate, and palmitate and oleate (the last 2 as complexes with 2% bovine plasma albumin). It is concluded that these substrates inhibit the phosphorylation of glucose in rat heart. The effects of these substrates on glucose phosphorylation are similar to those previously demonstrated in hearts from diabetic or starved rats. The effects of these substrates on glucose phosphorylation, like those of diabetes or starvation, are abolished by salicylate and by anoxia. When glucose uptake in the perfused rat heart is inhibited by fatty acids, detone bodies or pyruvate, the rate of glycolysis is markedly decreased, whereas the net synthesis of glycogen is either unchanged or increased. Similar effects of butyrate and of palmitate (carried by 0.85% bovine plasma albumin) on the uptake and metabolism of glucose in rat hemidiaphragms have been demonstrated. The output of C14O2 from [1-C14]glucose is greater than that from [6-C14]glucose in perfused rat heart, from which it is inferred that some glucose is oxidized through the pentose phosphate pathway in this tissue. The evidence for the possibility that fatty acids released in vitro from muscle glycerides in muscle from diabetic rats are responsible for impaired rates of glucose transport, glucose phosphorylation, glycolysis, fructose 6-phosphate phosphorylation and oxidation of pyruvate by pyruvate dehydrogenase is summarized and discussed.