Positron Emission Tomographic Measurements of Cerebral Glucose Utilization Using [1-<sup>11</sup>C]D-Glucose

Blomqvist, G.; Stone‐Elander, Sharon; Halldin, Christer; Roland, Per E.; Widén, L.; Lindqvist, M.; Swahn, Carl‐Gunnar; Långström, Bengt; Wiesel, F.-A.

doi:10.1038/jcbfm.1990.89

Cited by 52 publications

(26 citation statements)

References 42 publications

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“…Also, registration of human brain activation by voluntary hand movements with [ 18 F]FDG was about twice that with [ 11 C]glucose, 23% versus 12% respectively (Blomqvist et al, 1989, 1990, 1994). Hand movements caused a global reduction in the CMR O2 /CMR glc ratio and release from brain of 11 C-labelled acidic metabolites of [ 11 C]glucose to blood.…”

Section: Brain Activation In Normal Conscious Subjectsmentioning

confidence: 99%

Fueling and Imaging Brain Activation

2012

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Metabolic signals are used for imaging and spectroscopic studies of brain function and disease and to elucidate the cellular basis of neuroenergetics. The major fuel for activated neurons and the models for neuron–astrocyte interactions have been controversial because discordant results are obtained in different experimental systems, some of which do not correspond to adult brain. In rats, the infrastructure to support the high energetic demands of adult brain is acquired during postnatal development and matures after weaning. The brain's capacity to supply and metabolize glucose and oxygen exceeds demand over a wide range of rates, and the hyperaemic response to functional activation is rapid. Oxidative metabolism provides most ATP, but glycolysis is frequently preferentially up-regulated during activation. Underestimation of glucose utilization rates with labelled glucose arises from increased lactate production, lactate diffusion via transporters and astrocytic gap junctions, and lactate release to blood and perivascular drainage. Increased pentose shunt pathway flux also causes label loss from C1 of glucose. Glucose analogues are used to assay cellular activities, but interpretation of results is uncertain due to insufficient characterization of transport and phosphorylation kinetics. Brain activation in subjects with low blood-lactate levels causes a brain-to-blood lactate gradient, with rapid lactate release. In contrast, lactate flooding of brain during physical activity or infusion provides an opportunistic, supplemental fuel. Available evidence indicates that lactate shuttling coupled to its local oxidation during activation is a small fraction of glucose oxidation. Developmental, experimental, and physiological context is critical for interpretation of metabolic studies in terms of theoretical models.

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Section: Brain Activation In Normal Conscious Subjectsmentioning

confidence: 99%

Fueling and Imaging Brain Activation

2012

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“…Blomqvist et al 1990). The neglect of the loss of labelled metabolites other than 11CO2 implies that the tracer measures a quantity which is closer to the rate of oxidative than total glucose consumption ).…”

Section: Discussionmentioning

confidence: 99%

Facilitated transport of glucose from blood to brain in man and the effect of moderate hypoglycaemia on cerebral glucose utilization

Blomqvist¹,

Gjedde

Gutniak³

et al. 1991

Eur J Nucl Med

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The effect of steady-state moderate hypoglycaemia on human brain homeostasis has been studied with positron emission tomography using [U-11C]-D-glucose as tracer. To rule out any effects of insulin, the plasma insulin concentration was maintained at the same level under normo- and hypoglycaemic conditions. Reduction of blood glucose by 55% increased the glucose clearance through the blood-brain barrier by 50% and reduced brain glucose consumption by 40%. Blood flow was not affected. The results are consistent with facilitated transport of glucose from blood to brain in humans. The maximal transport rate of glucose from blood to brain was found to be 62 +/- 19 (mean +/- SEM) mumol hg-1 min-1, and the half-saturation constant was found to be 4.1 +/- 2.3 mM.

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“…11 C]glucose, efflux of labeled CO 2 to blood lagged behind the much larger efflux of unidentified 11 C-labeled acidic compounds, presumably mainly lactate; also, appearance of labeled CO 2 in blood was retarded when [1-14 C]glucose was the precursor compared with [U- 14 C]glucose, indicating that decarboxylation of carbon 1 via TCA cycle reactions was delayed compared with loss of carbons 3 and 4 of glucose in the pyruvate dehydrogenase (PDH) step, reflecting specific activity dilution by exchange of TCA cycle intermediates with the large pools of amino acids (Blomqvist et al, 1990). Thus, oxidative metabolism of lactate should be associated with label trapping unless lactate is metabolized in a small, isolated pool that does not mix with the amino acid pools ( Fig.…”

Section: What Is the Fate Of Glucose In Working Brain?mentioning

confidence: 98%

Glucose and lactate metabolism during brain activation

Dienel

Hertz

2001

J of Neuroscience Research

293

285

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The dependence of brain function on blood glucose as a fuel does not exclude the possibility that lactate within the brain might be transferred between different cell types and serve as an energy source. It has been recently suggested that 1) about 85% of glucose consumption during brain activation is initiated by aerobic glycolysis in astrocytes, triggered by demand for glycolytically derived energy for Na+ -dependent accumulation of transmitter glutamate and its amidation to glutamine, and 2) the generated lactate is quantitatively transferred to neurons for oxidative degradation. However, astrocytic glutamate uptake can be fueled by either glycolytically or oxidatively derived energy, and the extent to which "metabolic trafficking" of lactate might occur during brain function is unknown. In this review, the potential for an astrocytic-neuronal lactate flux has been estimated by comparing rates of glucose utilization in brain and in cultured neurons and astrocytes with those for lactate release and uptake. Working brain tissue and isolated brain cells release large amounts of lactate. Cellular lactate uptake occurs by carrier-mediated facilitated diffusion and is normally limited by its dependence on metabolism of accumulated lactate to maintain a concentration gradient. The rate of this process is similar in cultured astrocytes and glutamatergic neurons, and, at physiologically occurring lactate concentrations, lactate uptake corresponds at most to 25% of the rate of glucose oxidation, which accordingly is the upper limit for "metabolic trafficking" of lactate. Because of a larger local release than uptake of lactate and the necessity for rapid lactate clearance to maintain the intracellular redox state to support lactate production in the presence of normal oxygen levels, brain activation in vivo is probably, in many cases, accompanied by a substantial overflow of glycolytically generated lactate, both to different brain areas and under some conditions (spreading depression, hyperammonemia) to circulating blood.

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Positron Emission Tomographic Measurements of Cerebral Glucose Utilization Using [1-¹¹C]D-Glucose

Cited by 52 publications

References 42 publications

Fueling and Imaging Brain Activation

Fueling and Imaging Brain Activation

Facilitated transport of glucose from blood to brain in man and the effect of moderate hypoglycaemia on cerebral glucose utilization

Glucose and lactate metabolism during brain activation

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Positron Emission Tomographic Measurements of Cerebral Glucose Utilization Using [1-11C]D-Glucose

Cited by 52 publications

References 42 publications

Fueling and Imaging Brain Activation

Fueling and Imaging Brain Activation

Facilitated transport of glucose from blood to brain in man and the effect of moderate hypoglycaemia on cerebral glucose utilization

Glucose and lactate metabolism during brain activation

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Product

Resources

About

Positron Emission Tomographic Measurements of Cerebral Glucose Utilization Using [1-¹¹C]D-Glucose