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Paul Maruff - One of the best experts on this subject based on the ideXlab platform.
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Personality factors and cerebral Glucose Metabolism in community-dwelling older adults
Brain Structure and Function, 2020Co-Authors: Hamid R. Sohrabi, Kathryn Goozee, Michael Weinborn, Kaikai Shen, Belinda M. Brown, Stephanie R. Rainey-smith, Olivier Salvado, Kevin Taddei, Romola S. Bucks, Paul MaruffAbstract:Personality factors have been associated with Alzheimer’s disease (AD) and dementia, but they have not been examined against markers of regional brain Glucose Metabolism (a primary measure of brain functioning) in older adults without clinically diagnosed cognitive impairment. The relationship between personality factors derived from the five-factor model and cerebral Glucose Metabolism determined using positron emission tomography (PET) with [18F]-2-fluoro-2-deoxy- d -Glucose (18F-FDG-PET) was examined in a cohort of 237 non-demented, community-dwelling older adults aged 60–89 years (M ± SD = 73.76 ± 6.73). Higher neuroticism and lower scores on extraversion and conscientiousness were significantly associated with decreased Glucose Metabolism in brain regions typically affected by AD neuropathological processes, including the hippocampus and entorhinal cortex. Furthermore, while there were significant differences between apolipoprotein E ( APOE ) ε4 allele carriers and non-carriers on ^18F-FDG-PET results in the neocortex and other brain regions ( p
Theodore W. Kurtz - One of the best experts on this subject based on the ideXlab platform.
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transgenic and recombinant resistin impair skeletal muscle Glucose Metabolism in the spontaneously hypertensive rat
Journal of Biological Chemistry, 2003Co-Authors: Michal Pravenec, Vladimir Landa, Petr Mlejnek, Nianning Qi, Vaclav Zidek, Jiaming Wang, Petr Jansa, Ludmila Kazdova, Theodore W. KurtzAbstract:Abstract Increased serum levels of resistin, a molecule secreted by fat cells, have been proposed as a possible mechanistic link between obesity and insulin resistance. To further investigate the effects of resistin on Glucose Metabolism, we derived a novel transgenic strain of spontaneously hypertensive rats expressing the mouse resistin gene under the control of the fat-specific aP2 promoter and also performed in vitro studies of the effects of recombinant resistin on Glucose Metabolism in isolated skeletal muscle. Expression of the resistin transgene was detected by Northern blot analysis in adipose tissue and by real-time PCR in skeletal muscle and was associated with increased serum fatty acids and muscle triglycerides, impaired skeletal muscle Glucose Metabolism, and Glucose intolerance in the absence of any changes in serum resistin concentrations. In skeletal muscle isolated from non-transgenic spontaneously hypertensive rats, in vitro incubation with recombinant resistin significantly inhibited insulin-stimulated glycogenesis and reduced Glucose oxidation. These findings raise the possibility that autocrine effects of resistin in adipocytes, leading to release of other prodiabetic effector molecules from fat and/or paracrine actions of resistin secreted by adipocytes embedded within skeletal muscle, may contribute to the pathogenesis of disordered skeletal muscle Glucose Metabolism and impaired Glucose tolerance.
Richard M Caprioli - One of the best experts on this subject based on the ideXlab platform.
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regional differences in brain Glucose Metabolism determined by imaging mass spectrometry
Molecular metabolism, 2018Co-Authors: Andre Kleinridders, Heather A Ferris, Michelle L Reyzer, Michaela Rath, Marion Soto, Lisa M Manier, Jeffrey M Spraggins, Zhihong Yang, Robert Stanton, Richard M CaprioliAbstract:Abstract Objective Glucose is the major energy substrate of the brain and crucial for normal brain function. In diabetes, the brain is subject to episodes of hypo- and hyperglycemia resulting in acute outcomes ranging from confusion to seizures, while chronic metabolic dysregulation puts patients at increased risk for depression and Alzheimer's disease. In the present study, we aimed to determine how Glucose is metabolized in different regions of the brain using imaging mass spectrometry (IMS). Methods To examine the relative abundance of Glucose and other metabolites in the brain, mouse brain sections were subjected to imaging mass spectrometry at a resolution of 100 μm. This was correlated with immunohistochemistry, qPCR, western blotting and enzyme assays of dissected brain regions to determine the relative contributions of the glycolytic and pentose phosphate pathways to regional Glucose Metabolism. Results In brain, there are significant regional differences in Glucose Metabolism, with low levels of hexose bisphosphate (a glycolytic intermediate) and high levels of the pentose phosphate pathway (PPP) enzyme Glucose-6-phosphate dehydrogenase (G6PD) and PPP metabolite hexose phosphate in thalamus compared to cortex. The ratio of ATP to ADP is significantly higher in white matter tracts, such as corpus callosum, compared to less myelinated areas. While the brain is able to maintain normal ratios of hexose phosphate, hexose bisphosphate, ATP, and ADP during fasting, fasting causes a large increase in cortical and hippocampal lactate. Conclusion These data demonstrate the importance of direct measurement of metabolic intermediates to determine regional differences in brain Glucose Metabolism and illustrate the strength of imaging mass spectrometry for investigating the impact of changing metabolic states on brain function at a regional level with high resolution.
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Regional differences in brain Glucose Metabolism determined by imaging mass spectrometry
Elsevier, 2018Co-Authors: Andre Kleinridders, Heather A Ferris, Michelle L Reyzer, Michaela Rath, Marion Soto, Lisa M Manier, Jeffrey M Spraggins, Zhihong Yang, Robert C. Stanton, Richard M CaprioliAbstract:Objective: Glucose is the major energy substrate of the brain and crucial for normal brain function. In diabetes, the brain is subject to episodes of hypo- and hyperglycemia resulting in acute outcomes ranging from confusion to seizures, while chronic metabolic dysregulation puts patients at increased risk for depression and Alzheimer's disease. In the present study, we aimed to determine how Glucose is metabolized in different regions of the brain using imaging mass spectrometry (IMS). Methods: To examine the relative abundance of Glucose and other metabolites in the brain, mouse brain sections were subjected to imaging mass spectrometry at a resolution of 100 μm. This was correlated with immunohistochemistry, qPCR, western blotting and enzyme assays of dissected brain regions to determine the relative contributions of the glycolytic and pentose phosphate pathways to regional Glucose Metabolism. Results: In brain, there are significant regional differences in Glucose Metabolism, with low levels of hexose bisphosphate (a glycolytic intermediate) and high levels of the pentose phosphate pathway (PPP) enzyme Glucose-6-phosphate dehydrogenase (G6PD) and PPP metabolite hexose phosphate in thalamus compared to cortex. The ratio of ATP to ADP is significantly higher in white matter tracts, such as corpus callosum, compared to less myelinated areas. While the brain is able to maintain normal ratios of hexose phosphate, hexose bisphosphate, ATP, and ADP during fasting, fasting causes a large increase in cortical and hippocampal lactate. Conclusion: These data demonstrate the importance of direct measurement of metabolic intermediates to determine regional differences in brain Glucose Metabolism and illustrate the strength of imaging mass spectrometry for investigating the impact of changing metabolic states on brain function at a regional level with high resolution. Keywords: Brain imaging, Glucose Metabolism, Pentose phosphate pathway, Glycolysis, ATP, Mass spectrometr
Hamid R. Sohrabi - One of the best experts on this subject based on the ideXlab platform.
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Personality factors and cerebral Glucose Metabolism in community-dwelling older adults
Brain Structure and Function, 2020Co-Authors: Hamid R. Sohrabi, Kathryn Goozee, Michael Weinborn, Kaikai Shen, Belinda M. Brown, Stephanie R. Rainey-smith, Olivier Salvado, Kevin Taddei, Romola S. Bucks, Paul MaruffAbstract:Personality factors have been associated with Alzheimer’s disease (AD) and dementia, but they have not been examined against markers of regional brain Glucose Metabolism (a primary measure of brain functioning) in older adults without clinically diagnosed cognitive impairment. The relationship between personality factors derived from the five-factor model and cerebral Glucose Metabolism determined using positron emission tomography (PET) with [18F]-2-fluoro-2-deoxy- d -Glucose (18F-FDG-PET) was examined in a cohort of 237 non-demented, community-dwelling older adults aged 60–89 years (M ± SD = 73.76 ± 6.73). Higher neuroticism and lower scores on extraversion and conscientiousness were significantly associated with decreased Glucose Metabolism in brain regions typically affected by AD neuropathological processes, including the hippocampus and entorhinal cortex. Furthermore, while there were significant differences between apolipoprotein E ( APOE ) ε4 allele carriers and non-carriers on ^18F-FDG-PET results in the neocortex and other brain regions ( p
Nora D Volkow - One of the best experts on this subject based on the ideXlab platform.
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association between dopamine d4 receptor polymorphism and age related changes in brain Glucose Metabolism
PLOS ONE, 2013Co-Authors: Nora D Volkow, Dardo Tomasi, Genejack Wang, Frank Telang, Joanna S Fowler, Rita Z Goldstein, Nelly Klein, Christopher Wong, James M SwansonAbstract:Aging is associated with reductions in brain Glucose Metabolism in some cortical and subcortical regions, but the rate of decrease varies significantly between individuals, likely reflecting genetic and environmental factors and their interactions. Here we test the hypothesis that the variant of the dopamine receptor D4 (DRD4) gene (VNTR in exon 3), which has been associated with novelty seeking and sensitivity to environmental stimuli (negative and positive) including the beneficial effects of physical activity on longevity, influence the effects of aging on the human brain. We used positron emission tomography (PET) and [18F]fluoro-D-Glucose (18FDG) to measure brain Glucose Metabolism (marker of brain function) under baseline conditions (no stimulation) in 82 healthy individuals (age range 22–55 years). We determined their DRD4 genotype and found an interaction with age: individuals who did not carry the 7-repeat allele (7R−, n = 53) had a significant (p<0.0001) negative association between age and relative Glucose Metabolism (normalized to whole brain Glucose Metabolism) in frontal (r = −0.52), temporal (r = −0.51) and striatal regions (r = −0.47, p<0.001); such that older individuals had lower Metabolism than younger ones. In contrast, for carriers of the 7R allele (7R+ n = 29), these correlations with age were not significant and they only showed a positive association with cerebellar Glucose Metabolism (r = +0.55; p = 0.002). Regression slopes of regional brain Glucose Metabolism with age differed significantly between the 7R+ and 7R− groups in cerebellum, inferior temporal cortex and striatum. These results provide evidence that the DRD4 genotype might modulate the associations between regional brain Glucose Metabolism and age and that the carriers of the 7R allele appear to be less sensitive to the effects of age on brain Glucose Metabolism.
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low doses of alcohol substantially decrease Glucose Metabolism in the human brain
NeuroImage, 2006Co-Authors: Nora D Volkow, Genejack Wang, Joanna S Fowler, Christopher Wong, Panayotis K. Thanos, Dinko Franceschi, Laurence Maynard, John S Gatley, Richard L Veech, George KunosAbstract:Moderate doses of alcohol decrease Glucose Metabolism in the human brain, which has been interpreted to reflect alcohol-induced decreases in brain activity. Here, we measure the effects of two relatively low doses of alcohol (0.25 g/kg and 0.5 g/kg, or 5 to 10 mM in total body H2O) on Glucose Metabolism in the human brain. Twenty healthy control subjects were tested using positron emission tomography (PET) and FDG after placebo and after acute oral administration of either 0.25 g/kg, or 0.5 g/kg of alcohol, administered over 40 min. Both doses of alcohol significantly decreased whole-brain Glucose Metabolism (10% and 23% respectively). The responses differed between doses; whereas the 0.25 g/kg dose predominantly reduced Metabolism in cortical regions, the 0.5 g/kg dose reduced Metabolism in cortical as well as subcortical regions (i.e. cerebellum, mesencephalon, basal ganglia and thalamus). These doses of alcohol did not significantly change the scores in cognitive performance, which contrasts with our previous results showing that a 13% reduction in brain Metabolism by lorazepam was associated with significant impairment in performance on the same battery of cognitive tests. This seemingly paradoxical finding raises the possibility that the large brain metabolic decrements during alcohol intoxication could reflect a shift in the substrate for energy utilization, particularly in light of new evidence that blood-borne acetate, which is markedly increased during intoxication, is a substrate for energy production by the brain.