DIRECT ADMINISTRATION AND UTILIZATION OF [1-C-13]GLUCOSE BY FETAL BRAIN AND LIVER-TISSUES UNDER NORMAL AND ISCHEMIC CONDITIONS - H-1, P-31,AND C-13 NMR-STUDIES

Three distinct, maternal-independent routes (e,g, intraamniotic, intra peritoneal and intracerebral), for [1-C-13]glucose utilization by feta l brain and liver tissues, were examined by multinuclear magnetic reso nance (NMR) spectroscopy before and after vascular occlusion of the ma ternal-fetal blood flow. Labeled lactate was the major glycolytic prod uct by all routes, but in addition labeled TCA cycle products were als o generated, Fractional C-13 enrichment in both glucose and lactate we re always higher in the ischemic state compared to controls using eith er one of the three routes studied. After intraperitoneal injection to tal glucose in the fetal brain was decreased by 85% after 20 min reper fusion following 20 min ischemia, but was elevated up to 170% after 60 min, [1-C-13]glucose increased continuously by up to 370% after 60 mi n. Total glucose in the fetal liver remained unchanged while [1-C-13]g lucose increased up to 380%. Total lactate level in brain was 50-80% a bove the control apart from a transient increase (140%) notable after 40 min reperfusion. The kinetics of [3-C-13]lactate followed a similar time course. At the same time when lactate was transiently increased in fetal brain, total lactate as well as C-13-labeled lactate showed a transient decrease in liver after 40 min. While the ways of mobilizat ion of energy substrates for maintaining adequate metabolic activity i n the fetal brain remain still unclear, the present C-13 NMR studies s uggest that both liver glucose and lactate can contribute to brain met abolism particularly under ischemic stress. J. Neurosci, Res. 54:97-10 8, 1998. (C) 1998 Wiley-Liss, Inc.