期刊
METABOLISM-CLINICAL AND EXPERIMENTAL
卷 59, 期 1, 页码 100-106出版社
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.metabol.2009.07.012
关键词
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资金
- [RO1NS38672]
- [ROINS35192]
- [RO1DK62440]
- [P30NS057091]
- [P4IRR08679]
- [5 MO1 RR0400]
- NATIONAL CENTER FOR RESEARCH RESOURCES [P41RR008079, M01RR000400] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK062440] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [P30NS057091, R01NS038672, R01NS035192] Funding Source: NIH RePORTER
The aim of the present study was to use C-13 nuclear magnetic resonance (NMR) to measure the cerebral oxidative metabolic rate of glucose (CMRglc[ox]) in patients with diabetes and to compare these measurements with those collected from matched controls. We elected to study a group with type 1 diabetes mellitus and hypoglycemia unawareness because we had previously found such patients to have higher brain glucose concentrations than healthy volunteers under steady-state conditions. We sought to determine if this difference in steady-state brain concentrations could be explained by a difference in CMRglc(ox). Time courses of C-13 label incorporation in brain amino acids were measured in occipital cortex during infusion of [1-C-13]glucose. These time courses were fitted using a 1-compartment metabolic model to determine CMRglc(ox). Our results show that the tricarboxylic acid cycle (TCA) cycle rate (V-TCA, which is twice CMRglc[ox]) in subjects with type I diabetes mellitus was not significantly different from that of healthy controls (0.84 +/- 0.03 vs 0.79 +/- 0.03 mu mol/[g min], n = 5 in each group, mean +/- SEM). We conclude that the changes in steady-state brain glucose concentrations that we observed in patients with type I diabetes mellitus in a previous study (J Neurosci Res. 2005;79:42-47) cannot be explained by changes in oxidative glucose consumption (C) 2010 Elsevier Inc. All rights reserved.
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