Measurement of cerebral oxidative glucose consumption in patients with type 1 diabetes mellitus and hypoglycemia unawareness using (13)C nuclear magnetic resonance spectroscopy

The aim of the present study was to use (13)C 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 diab...

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Bibliographic Details
Published in:Metabolism, clinical and experimental clinical and experimental, 2010-01, Vol.59 (1), p.100-106
Main Authors: Henry, Pierre-Gilles, Criego, Amy B, Kumar, Anjali, Seaquist, Elizabeth R
Format: Article
Language:English
Subjects:
Adult
Awareness
Brain - metabolism
Carbon Isotopes
Case-Control Studies
Diabetes Mellitus, Type 1 - metabolism
Glucose - metabolism
Humans
Hypoglycemia - metabolism
Magnetic Resonance Spectroscopy - methods
Middle Aged
Models, Theoretical
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Summary:The aim of the present study was to use (13)C 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 (13)C label incorporation in brain amino acids were measured in occipital cortex during infusion of [1-(13)C]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 1 diabetes mellitus was not significantly different from that of healthy controls (0.84 +/- 0.03 vs 0.79 +/- 0.03 micromol/[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 1 diabetes mellitus in a previous study (J Neurosci Res. 2005;79:42-47) cannot be explained by changes in oxidative glucose consumption.
ISSN:1532-8600
DOI:10.1016/j.metabol.2009.07.012