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NMR study on [1‐ 13 C]glucose metabolism in the rat brain during hypoxia
Author(s) -
Fujiwara Naoshi,
Shimoji Koki,
Yuasa Tatsuhiko,
Igarashi Hironaka,
Miyatake Tadashi
Publication year - 1989
Publication title -
nmr in biomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.278
H-Index - 114
eISSN - 1099-1492
pISSN - 0952-3480
DOI - 10.1002/nbm.1940020305
Subject(s) - chemistry , oxygen , hypoxia (environmental) , metabolism , carbon 13 nmr , endocrinology , medicine , glutamine , carbohydrate metabolism , respiration , biochemistry , biology , stereochemistry , amino acid , anatomy , organic chemistry
The metabolism of [1‐ 13 C]glucose in the rat brain during hypoxia was investigated by 13 C NMR spectroscopy. Male Wistar rats, weighing 100–120 g, were anesthetized with ketamine (50 ˜ 75 mg/kg i.p.) and ventilated mechanically with a mixture of 30% oxygen, 69.5% nitrogen and 0.5% halothane. [1‐ 13 C]glucose (250 mg/kg) was infused twice, at 10 minute intervals, through the femoral vein. For the control group ( n = 4), the oxygen concentration of the inspiratory gas was maintained at 30% by vol throughout the experiments. For the hypoxia group ( n = 6), the oxygen concentration in the inspiratory gas was reduced to 6–7% (93–94% nitrogen) and maintained for 30 min following [1‐ 13 C]glucose infusion. 13 C NMR spectra were measured by a gated proton‐decoupling method without a nuclear Overhauser effect. The [1‐ 13 C]glucose infusion gave apparent signals of the C1 carbon in the α‐ and β‐anomers of [1‐ 13 C]glucose at 92.7 and 96.7 ppm, respectively. Signals of the C2, C3 and C4 carbon atoms in glutamate and/or glutamine (glx) also appeared at 55, 27 and 34 ppm, respectively. The intensity of glx‐C2 and glx‐C3 signals increased later than that of glx‐C4. The time lag between the different glx signals may reflect the turnover rate of the TCA cycle. Under the hypoxic condition, the signal of C3 carbon in lactate appeared at 21 ppm and increased. The α‐glucose signal diminished during hypoxia, whereas the β‐glucose signal kept its intensity. The difference in changes of the signal intensity between α‐ and β‐glucose suggests that α‐glucose is consumed more than β‐glucose in the hypoxic brain.