Literature DB >> 26755443

Uniform distributions of glucose oxidation and oxygen extraction in gray matter of normal human brain: No evidence of regional differences of aerobic glycolysis.

Fahmeed Hyder1, Peter Herman2, Christopher J Bailey3, Arne Møller4, Ronen Globinsky5, Robert K Fulbright5, Douglas L Rothman6, Albert Gjedde7.   

Abstract

Regionally variable rates of aerobic glycolysis in brain networks identified by resting-state functional magnetic resonance imaging (R-fMRI) imply regionally variable adenosine triphosphate (ATP) regeneration. When regional glucose utilization is not matched to oxygen delivery, affected regions have correspondingly variable rates of ATP and lactate production. We tested the extent to which aerobic glycolysis and oxidative phosphorylation power R-fMRI networks by measuring quantitative differences between the oxygen to glucose index (OGI) and the oxygen extraction fraction (OEF) as measured by positron emission tomography (PET) in normal human brain (resting awake, eyes closed). Regionally uniform and correlated OEF and OGI estimates prevailed, with network values that matched the gray matter means, regardless of size, location, and origin. The spatial agreement between oxygen delivery (OEF≈0.4) and glucose oxidation (OGI ≈ 5.3) suggests that no specific regions have preferentially high aerobic glycolysis and low oxidative phosphorylation rates, with globally optimal maximum ATP turnover rates (VATP ≈ 9.4 µmol/g/min), in good agreement with (31)P and (13)C magnetic resonance spectroscopy measurements. These results imply that the intrinsic network activity in healthy human brain powers the entire gray matter with ubiquitously high rates of glucose oxidation. Reports of departures from normal brain-wide homogeny of oxygen extraction fraction and oxygen to glucose index may be due to normalization artefacts from relative PET measurements.
© The Author(s) 2016.

Entities:  

Keywords:  Default mode network; PET; energy metabolism; fMRI; glutamate; neurophysiology

Mesh:

Substances:

Year:  2016        PMID: 26755443      PMCID: PMC4853838          DOI: 10.1177/0271678X15625349

Source DB:  PubMed          Journal:  J Cereb Blood Flow Metab        ISSN: 0271-678X            Impact factor:   6.200


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