Analysis of glucose metabolism by 18F-FDG-PET imaging and glucose transporter expression in a mouse model of intracerebral hemorrhage

Abstract

The relationship between cerebral glucose metabolism and glucose transporter expression after intracerebral hemorrhage (ICH) is unclear. Few studies have used positron emission tomography (PET) to explore cerebral glucose metabolism after ICH in rodents. In this study, we produced ICH in mice with an intrastriatal injection of collagenase to investigate whether glucose metabolic changes in 18F-fluoro-2-deoxy-D-glucose (FDG)-PET images are associated with expression of glucose transporters (GLUTs) over time. On days 1 and 3 after ICH, the ipsilateral striatum exhibited significant hypometabolism. However, by days 7 and 14, glucose metabolism was significantly higher in the ipsilateral striatum than in the contralateral striatum. The contralateral hemisphere did not show hypermetabolism at any time after ICH. Qualitative immunofluorescence and Western blotting indicated that the expression of GLUT1 in ipsilateral striatum decreased on days 1 and 3 after ICH and gradually returned to baseline by day 21. The 18F-FDG uptake after ICH was associated with expression of GLUT1 but not GLUT3 or GLUT5. Our data suggest that ipsilateral cerebral glucose metabolism decreases in the early stage after ICH and increases progressively in the late stage. Changes in 18F-FDG uptake on PET imaging are associated with the expression of GLUT1 in the ipsilateral striatum.

Vascular and neural transcriptomics reveal stage-dependent pathways to inflammation and cognitive dysfunction in a rat model of hypertension

“…In principle, these increased glucose consumption rates could be due to increased neuronal activity. Recent studies in both patients and animal models of dementia point also to activated microglia driving glucose hypermetabolism [105, 106], which is in line increased metabolic demands after experimental stroke and intracerebral hemorrhage (ICH), in which activated microglia and infiltrating inflammatory peripheral immune cells contribute to up to 50% of increased glucose consumption [107, 108]. The findings are discussed controversially, since activated microglia represent a rather small proportion of cells compared to the total number of cells in a volume-element in FDG-PET imaging and additionally reactive astrocytes have been suggested to play a role in elevated glucose consumption [109, 110].…”

Preparation and Bioevaluation of a Novel 99mTc-Labeled Glucose Derivative Containing Cyclohexane as a Promising Tumor Imaging Agent

“…As we know, [ 18 F]FDG and [ 99m Tc]Tc-EC-DG, which have entered clinical studies, have been proven to enter cells via GLUTs [16,[45][46][47]. For the purpose of exploring whether the uptake mechanism of the [ 99m Tc]Tc-CNMCHDG complex involves GULTs, D -glucose, L -glucose and insulin were added to cells to observe changes in the cellular uptake of the complex, respectively.…”

Study of the pathology and the underlying molecular mechanism of tissue injury around hematoma following intracerebral hemorrhage

“…ICH is an acute and severe disease of the central nervous system, which endangers the health of the public and brings a heavy burden on families and society ( 25 ). Current knowledge suggests that ICH not only includes primary lesions caused by hematoma (for example, hematoma formation and the placeholder effect of expansion, which causes direct damage to perihematoma tissue) but also includes agents indirectly responsible for secondary damage.…”

“…Current knowledge suggests that ICH not only includes primary lesions caused by hematoma (for example, hematoma formation and the placeholder effect of expansion, which causes direct damage to perihematoma tissue) but also includes agents indirectly responsible for secondary damage. These include toxic substances triggered by the burst of erythrocytes, a highly active metabolic state, spreading depression, oxidative stress, toxic effects of excitatory amino acids and inflammation in perihematoma tissue, which causes secondary damage ( 25 , 26 ). This is referred to as a microenvironment change in the perihematoma following ICH ( 1 , 4 , 12 ).…”

“…Cell component was associated with ‘extracellular region’ and ‘plasma membrane’. Therefore, based on GO functional annotation, it was possible to conclude that the changes in gene expression profiles in the peripheral hematoma region following ICH were primarily associated with external stimulation, which exerted harmful/beneficial effects, such as neuron protection/neuronal apoptosis, via activating ion channels (receptors) on the cell membrane and regulating the intracellular biological (stress) responses ( 25 – 27 ). Using IPA, enrichment of the classical signaling pathways of the differentially expressed genes in the post-ICH perihematoma was further studied.…”