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Journal articles on the topic 'Cerebral glucose metabolism'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Millichap, J. Gordon. "Cerebral Glucose Metabolism and ADHD." Pediatric Neurology Briefs 4, no. 11 (1990): 83. http://dx.doi.org/10.15844/pedneurbriefs-4-11-4.

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2

Rosenkrantz, Ted S., Anthony F. Philipps, Isabella Knox, et al. "Regulation of Cerebral Glucose Metabolism in Normal and Polycythemic Newborn Lambs." Journal of Cerebral Blood Flow & Metabolism 12, no. 5 (1992): 856–65. http://dx.doi.org/10.1038/jcbfm.1992.117.

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In contrast to previous investigations, a recent study of polycythemic lambs suggested that cerebral glucose delivery (concentration × blood flow), not arterial glucose concentration, determined cerebral glucose uptake. In the present study, the independent effects of arterial glucose concentration and delivery on cerebral glucose uptake were examined in two groups of chronically catheterized newborn lambs (control and polycythemic). Arterial glucose concentration was varied by an infusion of insulin. CBF was reduced in one group of lambs (polycythemic) by increasing the hematocrit. At all art

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3

Flatt, Emmanuelle, Bernard Lanz, Yves Pilloud, et al. "Measuring Glycolytic Activity with Hyperpolarized [2H7, U-13C6] D-Glucose in the Naive Mouse Brain under Different Anesthetic Conditions." Metabolites 11, no. 7 (2021): 413. http://dx.doi.org/10.3390/metabo11070413.

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Glucose is the primary fuel for the brain; its metabolism is linked with cerebral function. Different magnetic resonance spectroscopy (MRS) techniques are available to assess glucose metabolism, providing complementary information. Our first aim was to investigate the difference between hyperpolarized 13C-glucose MRS and non-hyperpolarized 2H-glucose MRS to interrogate cerebral glycolysis. Isoflurane anesthesia is commonly employed in preclinical MRS, but it affects cerebral hemodynamics and functional connectivity. A combination of low doses of isoflurane and medetomidine is routinely used in

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4

Cook, Edwin H., John Metz, Bennett L. Leventhal, et al. "Fluoxetine effects on cerebral glucose metabolism." NeuroReport 5, no. 14 (1994): 1745–48. http://dx.doi.org/10.1097/00001756-199409080-00014.

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5

Van Bogaert, P., D. Wikler, P. Damhaut, H. B. Szliwowski, and S. Goldman. "Cerebral glucose metabolism and centrotemporal spikes." Epilepsy Research 29, no. 2 (1998): 123–27. http://dx.doi.org/10.1016/s0920-1211(97)00072-7.

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6

McCall, Anthony L. "Cerebral glucose metabolism in diabetes mellitus." European Journal of Pharmacology 490, no. 1-3 (2004): 147–58. http://dx.doi.org/10.1016/j.ejphar.2004.02.052.

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7

Theodore, W. H., G. DiChiro, R. Margolin, D. Fishbein, R. J. Porter, and R. A. Brooks. "Barbiturates reduce human cerebral glucose metabolism." Neurology 36, no. 1 (1986): 60. http://dx.doi.org/10.1212/wnl.36.1.60.

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8

Theodore, William H. "Antiepileptic Drugs and Cerebral Glucose Metabolism." Epilepsia 29, s2 (1988): S48—S55. http://dx.doi.org/10.1111/j.1528-1157.1988.tb05797.x.

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9

Kim, Y. K., J. S. Kim, S.-H. Jeong, K.-S. Park, S. E. Kim, and S.-H. Park. "Cerebral glucose metabolism in Fisher syndrome." Journal of Neurology, Neurosurgery & Psychiatry 80, no. 5 (2009): 512–17. http://dx.doi.org/10.1136/jnnp.2008.154765.

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10

Rosenkrantz, T. S., I. Knox, E. L. Zalneraitis, et al. "Cerebral metabolism and electrocortical activity in the chronically hyperglycemic fetal lamb." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 265, no. 6 (1993): R1262—R1269. http://dx.doi.org/10.1152/ajpregu.1993.265.6.r1262.

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Previous studies in the fetal lamb have demonstrated that hyperglycemia stimulates the fetal metabolic rate. The present study examined the effects of chronic fetal hyperglycemia on fetal cerebral metabolic rate and electrocortical activity. Nine chronically instrumented fetal lambs had measurements of cerebral blood flow and cerebral uptake/excretion of oxygen, glucose, lactate, and beta-hydroxybutyrate taken before and during a 48-h fetal glucose infusion. Electrocortical activity was also recorded. The fetal arterial glucose concentration was 19.8 +/- 2.0 mg/dl before glucose infusion and 4

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11

Yu, Mi-Hee, Ji Sun Lim, Hyon-Ah Yi, Kyoung Sook Won, and Hae Won Kim. "Association between Visceral Adipose Tissue Metabolism and Cerebral Glucose Metabolism in Patients with Cognitive Impairment." International Journal of Molecular Sciences 25, no. 13 (2024): 7479. http://dx.doi.org/10.3390/ijms25137479.

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Visceral adipose tissue (VAT) dysfunction has been recently recognized as a potential contributor to the development of Alzheimer’s disease (AD). This study aimed to explore the relationship between VAT metabolism and cerebral glucose metabolism in patients with cognitive impairment. This cross-sectional prospective study included 54 patients who underwent 18F-fluorodeoxyglucose (18F-FDG) brain and torso positron emission tomography/computed tomography (PET/CT), and neuropsychological evaluations. VAT metabolism was measured by 18F-FDG torso PET/CT, and cerebral glucose metabolism was measured

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12

Yoshida, Koji, Kuniaki Ogasawara, Hiroaki Saura, et al. "Post-carotid endarterectomy changes in cerebral glucose metabolism on 18F-fluorodeoxyglucose positron emission tomography associated with postoperative improvement or impairment in cognitive function." Journal of Neurosurgery 123, no. 6 (2015): 1546–54. http://dx.doi.org/10.3171/2014.12.jns142339.

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OBJECT Cognitive function is often improved or impaired after carotid endarterectomy (CEA) for patients with cerebral hemodynamic impairment. Cerebral glucose metabolism measured using positron emission tomography (PET) with 18F-fluorodeoxyglucose (FDG) correlates with cognitive function in patients with neurodegenerative diseases. The present study aimed to determine whether postoperative changes in cerebral glucose metabolism are associated with cognitive changes after CEA. METHODS In patients who were scheduled to undergo CEA for ipsilateral internal carotid artery (ICA) stenosis (≥ 70% nar

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13

Hasselbalch, S. G., P. L. Madsen, L. P. Hageman, et al. "Changes in cerebral blood flow and carbohydrate metabolism during acute hyperketonemia." American Journal of Physiology-Endocrinology and Metabolism 270, no. 5 (1996): E746—E751. http://dx.doi.org/10.1152/ajpendo.1996.270.5.e746.

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During starvation, brain energy metabolism in humans changes toward oxidation of ketone bodies. To investigate if this shift is directly coupled to circulating blood concentrations of ketone bodies, we measured global cerebral blood flow (CBF) and global cerebral carbohydrate metabolism with the Kety-Schmidt technique before and during intravenous infusion with ketone bodies. During acute hyperketonemia (mean beta-hydroxybutyrate blood concentration 2.16 mM), cerebral uptake of ketones increased from 1.11 to 5.60 mumol.100 g-1.min-1, counterbalanced by an equivalent reduction of the cerebral g

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14

Orava, Janne, Lauri Nummenmaa, Tommi Noponen, et al. "Brown Adipose Tissue Function is Accompanied by Cerebral Activation in Lean But Not in Obese Humans." Journal of Cerebral Blood Flow & Metabolism 34, no. 6 (2014): 1018–23. http://dx.doi.org/10.1038/jcbfm.2014.50.

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Brown adipose tissue (BAT) is able to generate heat and dissipate energy in response to cold exposure in mammals. It has recently been acknowledged that adult humans also have functional BAT, whose metabolic activity is reduced in obesity. In healthy humans, the cerebral mechanisms that putatively control BAT function are unclear. By using positron emission tomography (PET), we showed that cold-induced BAT activation is associated with glucose metabolism in the cerebellum, thalamus, and cingulate, temporoparietal, lateral frontal, and occipital cortices in lean participants, whereas no such as

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15

Nagasawa, H., T. Imamura, H. Nomura, M. Itoh, and T. Ido. "A Case of Corticobasal Degeneration Studied with Positron Emission Tomography." Behavioural Neurology 6, no. 1 (1993): 59–64. http://dx.doi.org/10.1155/1993/657681.

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We measured cerebral blood flow, oxygen metabolism, glucose utilization, and dopamine metabolism in the brain of a patient with corticobasal degeneration using positron emission tomography (PET). The clinical picture is distinctive, comprising features referable to both cortical and basal ganglionic dysfunction. Brain imagings of glucose and dopamine metabolism can demonstrate greater abnormalities in the cerebral cortex and in the striatum contralateral to the more affected side than those of blood flow and oxygen metabolism. This unique combination study measuring both cerebral glucose utili

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16

Henriksen, Otto M., Mark B. Vestergaard, Ulrich Lindberg, et al. "Interindividual and regional relationship between cerebral blood flow and glucose metabolism in the resting brain." Journal of Applied Physiology 125, no. 4 (2018): 1080–89. http://dx.doi.org/10.1152/japplphysiol.00276.2018.

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Studies of the resting brain measurements of cerebral blood flow (CBF) show large interindividual and regional variability, but the metabolic basis of this variability is not fully established. The aim of the present study was to reassess regional and interindividual relationships between cerebral perfusion and glucose metabolism in the resting brain. Regional quantitative measurements of CBF and cerebral metabolic rate of glucose (CMRglc) were obtained in 24 healthy young men using dynamic [15O]H2O and [18F]fluorodeoxyglucose positron emission tomography (PET). Magnetic resonance imaging meas

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17

Bergeret, Sébastien, Mathieu Queneau, Mathieu Rodallec, et al. "Brain Glucose Metabolism in Cerebral Amyloid Angiopathy." Stroke 52, no. 4 (2021): 1478–82. http://dx.doi.org/10.1161/strokeaha.120.032905.

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Background and Purpose: The in vivo diagnosis of cerebral amyloid angiopathy (CAA) is currently based on the Boston criteria, which largely rely on hemorrhagic features on brain magnetic resonance imaging. Adding to these criteria 18 F-fluoro-deoxy-D-glucose (FDG) positron emission tomography, a widely available imaging modality, might improve their accuracy. Here we tested the hypothesis that FDG uptake is reduced in posterior cortical areas, particularly the primary occipital cortex, which pathologically bear the brunt of vascular Aβ deposition. Methods: From a large memory clinic database,

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18

Saxena, Sanjaya, Arthur L. Brody, Karron M. Maidment, et al. "Cerebral Glucose Metabolism in Obsessive-Compulsive Hoarding." American Journal of Psychiatry 161, no. 6 (2004): 1038–48. http://dx.doi.org/10.1176/appi.ajp.161.6.1038.

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19

Polinsky, R. J., H. Noble, G. Di Chiro, L. E. Nee, R. G. Feldman, and R. T. Brown. "Dominantly inherited Alzheimer's disease: cerebral glucose metabolism." Journal of Neurology, Neurosurgery & Psychiatry 50, no. 6 (1987): 752–57. http://dx.doi.org/10.1136/jnnp.50.6.752.

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20

Kim, Ji Soo, Seong-Hae Jeong, Hyun Seok Song, et al. "PO5.40 Cerebral Glucose Metabolism in Fisher Syndrome." Clinical Neurophysiology 120 (April 2009): S56. http://dx.doi.org/10.1016/s1388-2457(09)60180-2.

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21

Clark, C., H. Klonoff, and M. Hayden. "Regional Cerebral Glucose Metabolism in Turner Syndrome." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 17, no. 2 (1990): 140–44. http://dx.doi.org/10.1017/s0317167100030341.

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ABSTRACT:Regional cerebral glucose metabolism was examined in females with Turner syndrome, a sex chromosome abnormality. Previous studies have found a visual/spatial cognitive anomaly in these women but, to date, no abnormalities in brain structure or function have been associated with the condition. In the present study, decreases in regional metabolism were found in the occipital and parietal cortex. The involvement of the occipital cortex, although consistent with the observed cognitive anomalies, has not been suggested previously as an area dysfunction. Because the occipital cortex is a p

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22

Jacobsen, Leslie K., Susan D. Hamburger, John D. Van Horn, et al. "Cerebral glucose metabolism in childhood onset schizophrenia." Psychiatry Research: Neuroimaging 75, no. 3 (1997): 131–44. http://dx.doi.org/10.1016/s0925-4927(97)00050-4.

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23

Jacobsen, Leslie K., Susan D. Hamburger, John D. Van Hom, et al. "Cerebral glucose metabolism in childhood onset schizophrenia." Schizophrenia Research 24, no. 1-2 (1997): 166–67. http://dx.doi.org/10.1016/s0920-9964(97)82478-4.

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24

Clark, C. M., H. Klonoff, J. S. Tyhurst, et al. "Regional cerebral glucose metabolism in identical twins." Neuropsychologia 26, no. 4 (1988): 615–21. http://dx.doi.org/10.1016/0028-3932(88)90117-0.

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25

Buckley, P. F. "Cerebral Glucose Metabolism in Obsessive-Compulsive Hoarding." Yearbook of Psychiatry and Applied Mental Health 2006 (January 2006): 302–3. http://dx.doi.org/10.1016/s0084-3970(08)70292-5.

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26

Kerrigan, John F., Harry T. Chugani, and Michael E. Phelps. "Regional cerebral glucose metabolism in clinical subtypes of cerebral palsy." Pediatric Neurology 7, no. 6 (1991): 415–25. http://dx.doi.org/10.1016/0887-8994(91)90024-f.

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27

Richardson, B. S., A. R. Hohimer, J. M. Bissonnette, and C. M. Machida. "Insulin hypoglycemia, cerebral metabolism, and neural function in fetal lambs." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 248, no. 1 (1985): R72—R77. http://dx.doi.org/10.1152/ajpregu.1985.248.1.r72.

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The effect of insulin-induced hypoglycemia on cerebral oxidative metabolism (CMRO2) was studied in nine late gestational fetal lambs using the radiolabeled microsphere technique for cerebral blood flow and brachiocephalic to sagittal sinus blood O2 content differences. After 4 h insulin infusion to the fetus, arterial glucose fell from control levels of 0.96 +/- 0.11 (SE) to 0.69 +/- 0.09 mmol X l-1. CMRO2 was reduced from 199 +/- 23 to 155 +/- 22 mumol X 100 g-1 X min-1 (P less than 0.05), and cerebral glucose uptake fell from 31 +/- 4 to 25 +/- 4 mumol X 100 g-1 X min-1 (P less than 0.02). D

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28

Robertson, Claudia S., J. Clay Goodman, Raj K. Narayan, Charles F. Contant, and Robert G. Grossman. "The effect of glucose administration on carbohydrate metabolism after head injury." Journal of Neurosurgery 74, no. 1 (1991): 43–50. http://dx.doi.org/10.3171/jns.1991.74.1.0043.

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✓ The role of intravenous infusion of glucose in limiting ketogenesis and the effect of glucose on cerebral metabolism following severe head injury were studied in 21 comatose patients. The patients were randomly assigned to alimentation with or without glucose. Systemic protein wasting, arterial concentrations of energy substrates, and cerebral metabolism of these energy substrates were monitored for 5 days postinjury. Both groups were in negative nitrogen balance, and had wasting of systemic proteins despite substantial protein intake. Blood and cerebrospinal fluid (CSF) glucose concentratio

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29

Guilfoyle, Mathew R., Adel Helmy, Joseph Donnelly, et al. "Characterising the dynamics of cerebral metabolic dysfunction following traumatic brain injury: A microdialysis study in 619 patients." PLOS ONE 16, no. 12 (2021): e0260291. http://dx.doi.org/10.1371/journal.pone.0260291.

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Traumatic brain injury (TBI) is a major cause of death and disability, particularly amongst young people. Current intensive care management of TBI patients is targeted at maintaining normal brain physiology and preventing secondary injury. Microdialysis is an invasive monitor that permits real-time assessment of derangements in cerebral metabolism and responses to treatment. We examined the prognostic value of microdialysis parameters, and the inter-relationships with other neuromonitoring modalities to identify interventions that improve metabolism. This was an analysis of prospective data in

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30

Richardson, B. S., J. E. Patrick, J. Bousquet, J. Homan, and J. F. Brien. "Cerebral metabolism in fetal lamb after maternal infusion of ethanol." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 249, no. 5 (1985): R505—R509. http://dx.doi.org/10.1152/ajpregu.1985.249.5.r505.

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Cerebral uptake of glucose and O2 (VCO2) was measured in 10 chronically catheterized fetal lambs during a control period, after a 1-h maternal infusion of ethanol (1.0 g X kg-1 X h-1) and 1-h postethanol infusion, to determine if alterations in cerebral metabolism might occur. Brachiocephalic artery and sagittal vein blood samples were analyzed for glucose, O2 content, blood gases, pH, and ethanol. Cerebral blood flow (Qc) was measured with a radioactive microsphere technique. VCO2 decreased significantly, from 140 +/- 13 mumol X 100 g-1 X min-1 during the control period to 91 +/- 8 (P less th

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31

Nasrallah, Fatima A., Guilhem Pagès, Philip W. Kuchel, Xavier Golay, and Kai-Hsiang Chuang. "Imaging Brain Deoxyglucose Uptake and Metabolism by Glucocest MRI." Journal of Cerebral Blood Flow & Metabolism 33, no. 8 (2013): 1270–78. http://dx.doi.org/10.1038/jcbfm.2013.79.

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2-Deoxy-D-glucose (2DG) is a known surrogate molecule that is useful for inferring glucose uptake and metabolism. Although 13C-labeled 2DG can be detected by nuclear magnetic resonance (NMR), its low sensitivity for detection prohibits imaging to be performed. Using chemical exchange saturation transfer (CEST) as a signal-amplification mechanism, 2DG and the phosphorylated 2DG-6-phosphate (2DG6P) can be indirectly detected in 1H magnetic resonance imaging (MRI). We showed that the CEST signal changed with 2DG concentration, and was reduced by suppressing cerebral metabolism with increased gene

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32

McCall, A. L., I. Sussman, K. Tornheim, R. Cordero, and N. B. Ruderman. "Effects of hypoglycemia and diabetes on fuel metabolism by rat brain microvessels." American Journal of Physiology-Endocrinology and Metabolism 254, no. 3 (1988): E272—E278. http://dx.doi.org/10.1152/ajpendo.1988.254.3.e272.

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Glucose and beta-hydroxybutyrate metabolism were compared in isolated cerebral microvessels from chronically diabetic and hypoglycemic rats. As noted previously, glucose oxidation and conversion to lactate are diminished in rats with streptozotocin-induced diabetes. The decrease in glucose metabolism did not result from selective damage to diabetic vessels during isolation, since the ATP level and the ATP/ADP ratio were similar to those of nondiabetic rats, and O2 consumption was increased. In addition, cerebral microvessel oxidation of beta-hydroxybutyrate was enhanced by diabetes. By contras

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33

Andersen, Jens V., Sofie K. Christensen, Jakob D. Nissen, and Helle S. Waagepetersen. "Improved cerebral energetics and ketone body metabolism in db/db mice." Journal of Cerebral Blood Flow & Metabolism 37, no. 3 (2016): 1137–47. http://dx.doi.org/10.1177/0271678x16684154.

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It is becoming evident that type 2 diabetes mellitus is affecting brain energy metabolism. The importance of alternative substrates for the brain in type 2 diabetes mellitus is poorly understood. The aim of this study was to investigate whether ketone bodies are relevant candidates to compensate for cerebral glucose hypometabolism and unravel the functionality of cerebral mitochondria in type 2 diabetes mellitus. Acutely isolated cerebral cortical and hippocampal slices of db/db mice were incubated in media containing [U-13C]glucose, [1,2-13C]acetate or [U-13C]β-hydroxybutyrate and tissue extr

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34

Martin, W. R. Wayne, and Michael R. Hayden. "Cerebral Glucose and Dopa Metabolism in Movement Disorders." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 14, S3 (1987): 448–51. http://dx.doi.org/10.1017/s0317167100037896.

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ABSTRACT:The development of positron emission tomography (PET) has enabled us to perform in vivo measurements of certain aspects of regional cerebral function. Regional cerebral glucose metabolism may be readily quantified with [18F] fluoro-2-deoxyglucose (FDG) and presynaptic dopaminergic function may be studied with the labelled dopa analog 6-[18F] fluoro-L-dopa. We have applied a model to the analysis of 6-FD/PET data with which in vivo age-related changes in dopaminergic function may be demonstrated in normal subjects. With this technique, we have studied a series of asymptomatic MPTP-expo

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35

Wang, Andrew, Sarah C. Huen, Harding H. Luan, et al. "Glucose metabolism mediates disease tolerance in cerebral malaria." Proceedings of the National Academy of Sciences 115, no. 43 (2018): 11042–47. http://dx.doi.org/10.1073/pnas.1806376115.

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Sickness behaviors are a conserved set of stereotypic responses to inflammatory diseases. We recently demonstrated that interfering with inflammation-induced anorexia led to metabolic changes that had profound effects on survival of acute inflammatory conditions. We found that different inflammatory states needed to be coordinated with corresponding metabolic programs to actuate tissue-protective mechanisms. Survival of viral inflammation required intact glucose utilization pathways, whereas survival of bacterial inflammation required alternative fuel substrates and ketogenic programs. We thus

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36

Herbet, Mariola, Iwona Piątkowska-Chmiel, Monika Motylska, Monika Gawrońska-Grzywacz, Barbara Nieradko-Iwanicka, and Jarosław Dudka. "Alteration in the Expression of Genes Involved in Cerebral Glucose Metabolism as a Process of Adaptation to Stressful Conditions." Brain Sciences 12, no. 4 (2022): 498. http://dx.doi.org/10.3390/brainsci12040498.

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Exposure to chronic stress leads to disturbances in glucose metabolism in the brain, and changes in the functioning of neurons coexisting with the development of depression. The detailed molecular mechanism and cerebral gluconeogenesis during depression are not conclusively established. The aim of the research was to assess the expression of selected genes involved in cerebral glucose metabolism of mice in the validated animal paradigm of chronic stress. To confirm the induction of depression-like disorders, we performed three behavioral tests: sucrose preference test (SPT), forced swim test (

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37

Paulson, Olaf B., Steen G. Hasselbalch, Egill Rostrup, Gitte Moos Knudsen, and Dale Pelligrino. "Cerebral Blood Flow Response to Functional Activation." Journal of Cerebral Blood Flow & Metabolism 30, no. 1 (2009): 2–14. http://dx.doi.org/10.1038/jcbfm.2009.188.

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Cerebral blood flow (CBF) and cerebral metabolic rate are normally coupled, that is an increase in metabolic demand will lead to an increase in flow. However, during functional activation, CBF and glucose metabolism remain coupled as they increase in proportion, whereas oxygen metabolism only increases to a minor degree—the so-called uncoupling of CBF and oxidative metabolism. Several studies have dealt with these issues, and theories have been forwarded regarding the underlying mechanisms. Some reports have speculated about the existence of a potentially deficient oxygen supply to the tissue

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38

Kusaka, Takashi, Sonoko Ijichi, Yuka Yamamoto, and Yoshihiro Nishiyama. "Changes in cerebral glucose metabolism in newborn infants with cerebral infarction." Pediatric Neurology 32, no. 1 (2005): 46–49. http://dx.doi.org/10.1016/j.pediatrneurol.2004.06.012.

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39

Dickinson, C. John. "Cerebral Oxidative Metabolism in Hypertension." Clinical Science 91, no. 5 (1996): 539–50. http://dx.doi.org/10.1042/cs0910539.

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1. The evidence is now overwhelming that so-called ‘essential’ hypertension in man, i.e. high systemic arterial pressure for no apparent cause, is commonly initiated by increased efferent sympathetic activity directed to the cardiovascular system. Eventually structural and other changes take place in the heart, kidneys and blood vessels. These may reinforce, augment and even conceal the initially neurogenic background. The cause of the increased sympathetic activity remains in dispute, but it is probably not psychological in most cases. 2. The brain has a high requirement for energy — twice th

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40

Turbow, R. M., D. Curran-Everett, W. W. Hay, and M. D. Jones. "Cerebral lactate metabolism in near-term fetal sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 269, no. 4 (1995): R938—R942. http://dx.doi.org/10.1152/ajpregu.1995.269.4.r938.

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The present study was designed to see if lactate can cross the blood-brain barrier of the near-term fetal sheep and replace glucose as an oxidative substrate during normoglycemia and acute insulin-induced hypoglycemia. Cerebral uptake of glucose, oxygen, lactate, and [14C]lactate as well as cerebral production of 14CO2 were measured under three conditions: 1) normoglycemia-normolactemia, 2) acute hypoglycemia-normolactemia, and 3) hypoglycemia-steady-state hyperlactemia. Although uptake of tracer [14C]lactate was consistent, there was no net uptake of unlabeled lactate during either normoglyce

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41

Eguchi, Atsuko, Noriyuki Kimura, Yasuhiro Aso, et al. "Relationship Between the Japanese Version of the Montreal Cognitive Assessment and PET Imaging in Subjects with Mild Cognitive Impairment." Current Alzheimer Research 16, no. 9 (2019): 852–60. http://dx.doi.org/10.2174/1567205016666190805155230.

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Background: The Montreal Cognitive Assessment (MoCA) test has high sensitivity and specificity for detecting mild cognitive impairment or early dementia. How the MoCA score relates to findings of positron emission tomography imaging, however, remains unclear. <p></p> Objective: This prospective study examined the relationship between the Japanese version of the MoCA (MoCA-J) test and brain amyloid deposition or cerebral glucose metabolism among subjects with mild cognitive impairment. <p></p> Methods: A total of 125 subjects with mild cognitive impairment underwent the

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42

Ziegler, D., K. J. Langen, H. Herzog, et al. "Cerebral Glucose Metabolism in Type 1 Diabetic Patients." Diabetic Medicine 11, no. 2 (1994): 205–9. http://dx.doi.org/10.1111/j.1464-5491.1994.tb02021.x.

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Hurwitz, T. A., C. Clark, E. Murphy, H. Klonoff, W. R. W. Martin, and B. D. Pate. "Regional Cerebral Glucose Metabolism in Major Depressive Disorder." Canadian Journal of Psychiatry 35, no. 8 (1990): 684–88. http://dx.doi.org/10.1177/070674379003500807.

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44

Bisaga, Adam, Jack L. Katz, Angelo Antonini, et al. "Cerebral Glucose Metabolism in Women With Panic Disorder." American Journal of Psychiatry 155, no. 9 (1998): 1178–83. http://dx.doi.org/10.1176/ajp.155.9.1178.

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45

Knapp, W. H. "Pathomechanisms of the Cerebral and Myocardial Glucose Metabolism." Nuklearmedizin 29, no. 06 (1990): 236–45. http://dx.doi.org/10.1055/s-0038-1629538.

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Walsh, Sharon L., Stephen F. Gilson, Donald R. Jasinski, et al. "Buprenorphine Reduces Cerebral Glucose Metabolism in Polydrug Abusers." Neuropsychopharmacology 10, no. 3 (1994): 157–70. http://dx.doi.org/10.1038/npp.1994.18.

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Blesa, R., E. Mohr, R. S. Miletich, et al. "Changes in cerebral glucose metabolism with normal aging." European Journal of Neurology 4, no. 1 (1997): 8–14. http://dx.doi.org/10.1111/j.1468-1331.1997.tb00294.x.

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Theodore, William H., Kathey Kelley, Maria T. Toczek, and William D. Gaillard. "Epilepsy Duration, Febrile Seizures, and Cerebral Glucose Metabolism." Epilepsia 45, no. 3 (2004): 276–79. http://dx.doi.org/10.1111/j.0013-9580.2004.51803.x.

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Tedeschi, E., S. G. Hasselbalch, G. Waldemar, et al. "Heterogeneous cerebral glucose metabolism in normal pressure hydrocephalus." Journal of Neurology, Neurosurgery & Psychiatry 59, no. 6 (1995): 608–15. http://dx.doi.org/10.1136/jnnp.59.6.608.

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Ma, A. "2.036 CEREBRAL GLUCOSE METABOLISM IN PROGRESSIVE SUPRANUCLEAR PALSY." Parkinsonism & Related Disorders 18 (January 2012): S100. http://dx.doi.org/10.1016/s1353-8020(11)70469-2.

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