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在脂肪肝模型中,利用体内31P磁共振波谱(31P-MRS)和19F磁共振波谱(19F-MRS)研究肝损伤对果糖和5-氟尿嘧啶代谢的影响。

Effects of hepatic impairment on the metabolism of fructose and 5-fluorouracil, as studied in fatty liver models using in vivo 31P-MRS and 19F-MRS.

作者信息

Otsuka H, Harada M, Koga K, Nishitani H

机构信息

Department of Radiology, Tokushima University, Japan.

出版信息

Magn Reson Imaging. 1999 Feb;17(2):283-90. doi: 10.1016/s0730-725x(98)00077-0.

Abstract

The purpose of this study was to observe the effects of hepatic impairment on the metabolism of fructose and 5-fluorouracil (5-FU) in fatty liver models using in vivo 31P-MRS and 19F-MRS and to compare the results. In addition, we compared the results to those of other conventional tests such as laboratory examinations, imaging and pathology. Male SIc:Wistar rats were examined on BEM170/200 (4.7 T, Otsuka Electronics, USA) with 17-mm diameter surface coil. Fatty liver was induced by a choline deficient diet (CD diet) for 2 weeks. 31P-MRS were obtained for 90 min after intravenous (i.v.) injection of 1 g/kg of fructose and 19F-MRS were measured for 100 min after i.v. injection of 100 mg/kg of 5-FU. 1H-MRS and 1H-MRI were also performed. On 31P-MRS, there was no statistical difference in the time course of phosphomonoester (PME), adenosine triphosphate (ATP), and inorganic phosphate (Pi) between CD diet group and control group. On 19F-MRS, we detected high peak of fluoronucleotide (Fnct) and suppressed peak of alpha-fluoro-beta-alanine (FBAL) in CD diet group. We showed the metabolism of fructose and 5-FU by 31P-MRS and 19F-MRS, respectively. There was no difference in fructose metabolism but we observed increased fluoronucleotide and decreased a-fluoro-b-alanine in 5-FU metabolism of fatty liver. We speculate that the effects of hepatic impairment in fatty liver may be more severe on 5-FU metabolism and the increased fluoronucleotide may reflect cell proliferation.

摘要

本研究的目的是使用体内31P磁共振波谱(MRS)和19F MRS观察肝损伤对脂肪肝模型中果糖和5-氟尿嘧啶(5-FU)代谢的影响,并比较结果。此外,我们将结果与其他传统检测方法(如实验室检查、影像学和病理学)的结果进行了比较。雄性SIc:Wistar大鼠在配备17毫米直径表面线圈的BEM170/200(4.7T,大冢电子,美国)上进行检查。通过胆碱缺乏饮食(CD饮食)诱导脂肪肝2周。静脉注射1g/kg果糖后90分钟获取31P MRS,静脉注射100mg/kg 5-FU后100分钟测量19F MRS。还进行了1H MRS和1H磁共振成像(MRI)。在31P MRS上,CD饮食组和对照组之间的磷酸单酯(PME)、三磷酸腺苷(ATP)和无机磷酸盐(Pi)的时间进程没有统计学差异。在19F MRS上,我们在CD饮食组中检测到氟核苷酸(Fnct)的高峰和α-氟-β-丙氨酸(FBAL)的抑制峰。我们分别通过31P MRS和19F MRS展示了果糖和5-FU的代谢。果糖代谢没有差异,但我们观察到脂肪肝的5-FU代谢中氟核苷酸增加,α-氟-β-丙氨酸减少。我们推测肝损伤在脂肪肝中对5-FU代谢的影响可能更严重,并且氟核苷酸的增加可能反映细胞增殖。

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