Regulation of hepatic inorganic phosphate and ATP in response to fructose loading: an in vivo 31P-NMR study.
Regulation of hepatic inorganic phosphate and ATP in response to fructose loading: an in vivo 31P-NMR study.
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果糖负荷对肝无机磷酸盐和 ATP 的调节：体内 31P-NMR 研究。
DOI：
10.1016/0167-4889(89)90084-0
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Weiner,MW
中科院分区：
文献类型：
--
作者：
Karczmar,GS;Kurtz,T;Tavares,NJ;Weiner,MW
果糖负荷导致1-磷酸果糖（Fru 1 P）在肝脏中蓄积。本实验的目标是：首先，区分ATP，胞内无机磷酸盐（Pi），和细胞外皮亚斯来源的磷酸盐磷酸化的果糖，第二，检查ATP和Fru 1 Pon运动的影响磷酸盐进出这三个池。为了实现这些目标，使用31 P-NMR监测肝脏ATP、Pi和Fru 1 P对连续两次注射果糖的反应。第一组给予对照水平的ATP，第二组在第一组后1小时给予对照水平65%的ATP。通过将NMR可检测的总磷和NMR可检测的Pi与血浆Pi的测量值相关联来区分细胞内和细胞外Pi的变化。最初的果糖注射导致Fru 1 P的快速积累，血浆和NMR可检测到的Pi的小幅下降以及ATP的急剧下降。总NMR检测磷没有变化，表明磷酸盐没有进入或离开肝脏。因此，Fru 1 P的积累最初通过ATP的等量减少来平衡，而Pi没有大的变化。在第二次注射后，当ATP为对照的65%时，Fru 1 P以与第一次注射后大致相同的速率和水平积累。ATP几乎没有进一步的变化，NMR可检测到的Pi显著降低，而血浆Pi高于第一次注射后。因此，第二次注射后NMR可检测的Pi的更大降低代表细胞内Pi的显著降低。返回的Fru 1 P控制与血浆Pi的急剧增加，并减少总NMR可检测的磷酸盐。这表明从Fru 1 Pin释放的磷酸盐进入细胞外空间。这些数据表明细胞内PI调节的机制。当有足够的ATP可用时，ATP水解为Fru 1 P的合成提供磷酸盐，并防止细胞内Pi的显著降低。当ATP减少时，Fru 1 P的积累消耗细胞内的Pi。因此，ATP可用性的降低与细胞内Pi利用率的增加相关。当Fru 1 Preturn为对照时，细胞内Pi的增加受到Pi释放到血浆中的限制。
Fructose loading results in hepatic accumulation of fructose 1-phosphate (Fru1P). The goals of the present experiments were: first, to distinguish between ATP, intracellular inorganic phosphate (Pi), and extracellular Pias sources of phosphate for the phosphorylation of fructose, and second, to examine the influence of ATP and Fru1Pon movement of phosphate into and out of these three pools. To achieve these goals,31P-NMR was used to monitor the response of hepatic ATP, Piand Fru1Pto two consecutive injections of fructose. The first was administered with ATP at the control level, and the second, 1 h after the first, with ATP at 65% of the control level. Changes in intra- and extracellular Piwere distinguished by correlating measurements of total NMR-detectable phosphorus and NMR-detectable Piwith measurements of plasma Pi. The initial fructose injection resulted in rapid accumulation of Fru1P, small decreases in plasma and NMR-detectable Piand a dramatic decrease in ATP. Total NMR-detectable phosphorus did not change, suggesting that phosphate did not enter or leave the liver. Therefore, accumulation of Fru1Pwas initially balanced by an equivalent decrease in ATP, without large changes in Pi. Following the second injection, when ATP was at 65% of control, Fru1Paccumulated at approximately the same rate and to the same level as achieved following the first injection. There was little further change in ATP and a marked decrease in NMR-detectable Pi, while plasma Piwas higher than after the first injection. Therefore the greater decrease in NMR-detectable Pifollowing the second injection represented a significant decrease in intracellular Pi. Return of Fru1Pto control coincided with a dramatic increase in plasma Pi, and a decrease in total NMR-detectable phosphate. This suggests that phosphate released from Fru1Pentered the extracellular space. These data suggest the mechanisms by which intracellular Piis regulated. When sufficient ATP is available, ATP hydrolysis supplies phosphate for the synthesis of Fru1P, and prevents a significant decrease in intracellular Pi. When ATP is reduced, accumulation of Fru1Pdepletes intracellular Pi. Therefore, decreased availability of ATP correlates with increased utilization of intracellular Pi. When Fru1Preturns to control, the increase in intracellular Piis limited by release of Piinto the plasma.
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影响因子：
56.9
作者：
MAENPAA, PH;RAIVIO, KO;KEKOMAKI, MP
通讯作者：
KEKOMAKI, MP
31-P NMR 在体内肝脏代谢研究中的应用
DOI：
--
发表时间：
1983
期刊：
Pharmacology, Biochemistry and Behavior
影响因子：
--
作者：
Bjørn Quistorff;A. Engkagul;Britton Chance
通讯作者：
Britton Chance
31 P NMR 测定肝脏代谢
影响因子：
4
作者：
R. Iles;J. Griffiths
通讯作者：
J. Griffiths
DOI：
--
发表时间：
1974
期刊：
Biochimica et Biophysica Acta
影响因子：
--
作者：
L. Sestoft
通讯作者：
L. Sestoft
D-果糖诱导的肝脏腺嘌呤核苷酸消耗。
影响因子：
5.8
作者：
Kari O. Raivio;Martti Kekomäki;P. Mäenpää
通讯作者：
P. Mäenpää