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Direct administration and utilization of [1‐ 13 C]glucose by fetal brain and liver tissues under normal and ischemic conditions: 1 H, 31 P, and 13 C NMR studies
Author(s) -
Brand Annette,
Gil Shosh,
Leibfritz Dieter,
Yavin Ephraim
Publication year - 1998
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19981001)54:1<97::aid-jnr10>3.0.co;2-6
Subject(s) - fetus , lactic acid , medicine , endocrinology , ischemia , intraperitoneal injection , metabolism , chemistry , carbohydrate metabolism , carbon 13 nmr , blood flow , biology , pregnancy , stereochemistry , genetics , bacteria
Three distinct, maternal‐independent routes (e.g. intraamniotic, intraperitoneal and intracerebral), for [1‐ 13 C]glucose utilization by fetal brain and liver tissues, were examined by multinuclear magnetic resonance (NMR) spectroscopy before and after vascular occlusion of the maternal‐fetal blood flow. Labeled lactate was the major glycolytic product by all routes, but in addition labeled TCA cycle products were also generated. Fractional 13 C enrichment in both glucose and lactate were always higher in the ischemic state compared to controls using either one of the three routes studied. After intraperitoneal injection total glucose in the fetal brain was decreased by 85% after 20 min reperfusion following 20 min ischemia, but was elevated up to 170% after 60 min. [1‐ 13 C]glucose increased continuously by up to 370% after 60 min. Total glucose in the fetal liver remained unchanged while [1‐ 13 C]glucose increased up to 380%. Total lactate level in brain was 50–80% above the control apart from a transient increase (140%) notable after 40 min reperfusion. The kinetics of [3‐ 13 C]lactate followed a similar time course. At the same time when lactate was transiently increased in fetal brain, total lactate as well as 13 C‐labeled lactate showed a transient decrease in liver after 40 min. While the ways of mobilization of energy substrates for maintaining adequate metabolic activity in the fetal brain remain still unclear, the present 13 C NMR studies suggest that both liver glucose and lactate can contribute to brain metabolism particularly under ischemic stress. J. Neurosci. Res. 54:97–108, 1998. © 1998 Wiley‐Liss, Inc.