In vivo and in vitro 31P magnetic resonance spectroscopic studies of the hepatic response of healthy rats and rats with acute hepatic damage to fructose loading

In vivo and in vitro 31P magnetic resonance spectroscopic studies of the hepatic response of healthy rats and rats with acute hepatic damage to fructose loading
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健康大鼠和急性肝损伤大鼠对果糖负荷肝反应的体内外31P磁共振波谱研究

DOI:
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发表时间:
1994
影响因子:
3.3
通讯作者:
M. Brauer
M. Brauer
中科院分区:
医学3区
文献类型:
--
作者:
Wuhua Lu;S. Locke;M. Brauer

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使用动态体内 31P MRS 比较对照大鼠和接受急性亚致死剂量四氯化碳 (CCI4) 或溴苯 (BB) 的大鼠对果糖激发的肝脏反应。使用果糖负荷条件,其中对照大鼠在施用果糖后仅表现出肝磷酸单酯(PME)适度增加,并且ATP、Pi和细胞内pH小幅下降。 CCI4 和 BB 处理的大鼠均表现出比对照组大鼠更多的果糖诱导的 PME 积累。 Trolox C 是一种自由基清除剂,可以阻止大部分 PME 的增加。接受 BB 治疗的大鼠,给予足够的时间从肝毒性损伤中恢复,对果糖负荷的反应与对照组类似。对照、毒物处理大鼠和毒物加 Trolox C 处理大鼠的肝脏醛缩酶活性与果糖负荷后 PME 积累呈负相关(相关系数:-0.834,P < 0.05)。通过体外 31P MRS 研究的大鼠肝脏高氯酸提取物证实,果糖负载后 PME 的积累主要是由于果糖 1-磷酸的增加。这些研究与醛缩酶催化的 1-磷酸果糖裂解是肝脏果糖代谢的速率限制一致,并且 CCI 和 BB 治疗修饰并灭活了醛缩酶。
The hepatic response to a fructose challenge for control rats, and rats subjected to an acute sublethal dose of carbon tetrachloride (CCI4) or bromobenzene (BB), was compared using dynamic in vivo 31P MRS. Fructose loading conditions were used in which control rats showed only a modest increase in hepatic phosphomonoester (PME), and a small decrease in ATP, Pi, and intracellular pH after fructose administration. Both CCI4, and BB‐treated rats showed a much greater fructose‐induced accumulation of PME than did controls. Trolox C, a free radical scavenger, prevented most of this PME increase. BB‐treated rats, given sufficient time to recover from the hepa‐totoxic insult, responded to the fructose load similarly to controls. Liver aldolase activities of control, toxicant‐treated rats, and toxicant plus Trolox C‐treated rats correlated inversely with PME accumulation after fructose loading (correlation coefficient: −0.834, P < 0.05). Perchloric acid extracts of rat livers studied by in vitro 31P MRS confirmed that the PME accumulation after fructose loading is mainly due to an increase in fructose 1‐phosphate. These studies are consistent with the aldolase‐catalyzed cleavage of fructose 1‐phosphate being rate‐limiting in hepatic fructose metabolism, and that the CCI, and BB treatment modify and inactivate the aldolase enzyme.
通过 31P-NMR 检测果糖负载后腺嘌呤对肝核苷酸的影响。
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