FRUCTOSE 2,6-BISPHOSPHATE CHANGES IN RAT-BRAIN DURING ISCHEMIA

被引：11

作者：

YAMAMOTO, M

HAMASAKI, N

MARUTA, Y

TOMONAGA, M

机构：

[1] FUKUOKA UNIV, SCH MED,DEPT CLIN CHEM & LAB MED,7-45-1 NANAKUMA, JONAN KU, FUKUOKA 81401, JAPAN

[2] FUKUOKA UNIV, SCH MED, DEPT NEUROSURG, FUKUOKA 81401, JAPAN

来源：

JOURNAL OF NEUROCHEMISTRY | 1990年 / 54卷 / 02期

关键词：

Brain ischemia; Fructose 2,6‐bisphosphate; Glycolysis regulation;

D O I：

10.1111/j.1471-4159.1990.tb01912.x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Brain ischemia was produced by bilateral ligation of the common carotid arteries of spontaneously hypertensive rats. The concentrations of fructose 2,6‐bisphosphate and other glycolytic intermediates as well as of pyridine and adenine nucleotides were measured in frozen brain samples. In contrast to the decrease reported in hepatocytes under anoxic conditions, the fructose 2,6‐bisphosphate content was increased by 20–30% during the early stages of ischemia. Elevation in fructose 1,6‐bisphosphate level and lactate formation followed the rise in fructose 2,6‐bisphosphate content, a finding suggesting that this compound plays a key role in the compensatory acceleration of glycolysis under ischemic conditions in vivo. Copyright © 1990, Wiley Blackwell. All rights reserved

引用

页码：592 / 597

页数：6

共 28 条

[1] ENERGY-REQUIRING CELL FUNCTIONS IN THE ISCHEMIC BRAIN - THEIR CRITICAL SUPPLY AND POSSIBLE INHIBITION IN PROTECTIVE THERAPY [J].