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

• 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
• ISSN: 1532-8600
• DOI: 10.1016/j.metabol.2009.07.012

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.