scholarly journals Ketamine ameliorates depressive-like behaviors in mice through increasing glucose uptake regulated by the ERK/GLUT3 signaling pathway

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xin Ouyang ◽  
Zhengjia Wang ◽  
Mei Luo ◽  
Maozhou Wang ◽  
Xing Liu ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Glucose Uptake ◽  
Glucose Transporter ◽  
Signal Pathway ◽  
Mild Stress ◽  
Expression Levels ◽  
Immobility Time ◽  
Lactic Acid Content ◽  
The Brain ◽  
Glut Expression

AbstractTo investigate the effects of ketamine on glucose uptake and glucose transporter (GLUT) expression in depressive-like mice. After HA1800 cells were treated with ketamine, 2-[N-(7-Nitrobenz-2-oxa-1,3-diazol-4-yl)Amino]-2-Deoxyglucose (2-NBDG) was added to the cells to test the effects of ketamine on glucose uptake, production of lactate, and expression levels of GLUT, ERK1/2, AKT, and AMPK. Adult female C57BL/6 mice were subjected to chronic unpredictable mild stress (CUMS), 27 CUMS mice were randomly divided into the depression, ketamine (i.p.10 mg/kg), and FR180204 (ERK1/2 inhibitor, i.p.100 mg/kg) + ketamine group. Three mice randomly selected from each group were injected with 18F-FDG at 6 h after treatment. The brain tissue was collected at 6 h after treatment for p-ERK1/2 and GLUTs. Treatment with ketamine significantly increased glucose uptake, extracellular lactic-acid content, expression levels of GLUT3 and p-ERK in astrocytes and glucose uptake in the prefrontal cortex (P < 0.05), and the immobility time was significantly shortened in depressive-like mice (P < 0.01). An ERK1/2 inhibitor significantly inhibited ketamine-induced increases in the glucose uptake in depressive-like mice (P < 0.05), as well as prolonged the immobility time (P < 0.01). The expression levels of p-ERK1/2 and GLUT3 in depressive-like mice were significantly lower than those in normal control mice (P < 0.01). Ketamine treatment in depressive-like mice significantly increased the expression levels of p-ERK1/2 and GLUT3 in the prefrontal cortex (P < 0.01), whereas an ERK1/2 inhibitor significantly inhibited ketamine-induced increases (P < 0.01).Our present findings demonstrate that ketamine mitigated depressive-like behaviors in female mice by activating the ERK/GLUT3 signal pathway, which further increased glucose uptake in the prefrontal cortex.

β-Carboline harmine reverses the effects induced by stress on behaviour and citrate synthase activity in the rat prefrontal cortex

2013 ◽  
Vol 25 (6) ◽  
pp. 328-333 ◽  
Author(s):  
Helena Mendes Abelaira ◽  
Gislaine Zilli Réus ◽  
Giselli Scaini ◽  
Emilio Luiz Streck ◽  
José Alexandre Crippa ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Energy Metabolism ◽  
Citrate Synthase ◽  
Memory Performance ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Sucrose Intake ◽  
The Brain

ObjectivesThe present study was aimed at evaluating the effects of the administration of β-carboline harmine on behaviour and citrate synthase activity in the brain of rats exposed to chronic mild stress (CMS) procedure.MethodsTo this aim, after 40 days of exposure to CMS procedure, rats were treated with harmine (15 mg/kg/day) for 7 days, then memory, anhedonia and citrate synthase activity were assessed.ResultOur findings demonstrated that stressed rats treated with saline increased the sucrose intake, and the stressed rats treated with harmine reversed this effect. Neither stress nor harmine treatment altered memory performance in rats. In addition, chronic stressful situations induced increase in citrate synthase activity in the prefrontal cortex, but not in the hippocampus and striatum. Treatment with harmine reversed the increase in citrate synthase activity in the prefrontal cortex.ConclusionThese findings support the hypothesis that harmine could be involved in controlling the energy metabolism.

scholarly journals Regulation of GLUT Transporters by Flavonoids in Androgen-Sensitive and -Insensitive Prostate Cancer Cells

Endocrinology ◽  
2014 ◽  
Vol 155 (9) ◽  
pp. 3238-3250 ◽  
Author(s):  
Pedro Gonzalez-Menendez ◽  
David Hevia ◽  
Aida Rodriguez-Garcia ◽  
Juan C. Mayo ◽  
Rosa M. Sainz
Keyword(s):  
Prostate Cancer ◽  
Glucose Uptake ◽  
Cancer Cells ◽  
Subcellular Distribution ◽  
Glucose Transporter ◽  
Docking Simulation ◽  
Prostate Cancer Cells ◽  
Protein Levels ◽  
Glucose Binding ◽  
Glut Expression

Abstract Cancer cells show different metabolic requirements from normal cells. In prostate cancer, particularly, glycolytic metabolism differs in androgen-responsive and nonresponsive cells. In addition, some natural compounds with antiproliferative activities are able to modify glucose entry into cells by either modulating glucose transporter (GLUT) expression or by altering glucose binding. The aim of this work was to study the regulation of some GLUTs (GLUT1 and GLUT4) in both androgen-sensitive (LNCaP) and -insensitive (PC-3) prostate cancer cells by 4 structurally different flavonoids (ie, genistein, phloretin, apigenin, and daidzein). Glucose uptake was measured using nonradiolabeled 2-deoxyglucose. The evaluation of protein levels as well as subcellular distribution of GLUT1/4 were analyzed by Western blot and immunocytochemistry, respectively. Androgen-insensitive LNCaP-R and androgen-sensitive PC-3-AR cells were used to study the effect of androgen signaling. Additionally, a docking simulation was employed to compare interactions between flavonoids and XylE, a bacterial homolog of GLUT1 to -4. Results show for the first time the presence of functionally relevant GLUT4 in prostate cancer cells. Furthermore, differences in GLUT1 and GLUT4 levels and glucose uptake were found, without differences on subcellular distribution, after incubation with flavonoids. Docking simulation showed that all compounds interact with the same location of transporters. More importantly, differences between androgen-sensitive and -insensitive prostate cancer cells were found in both GLUT protein levels and glucose uptake. Thus, phenotypic characteristics of prostate cancer cells are responsible for the different effects of these flavonoids in glucose uptake and in GLUT expression rather than their structural differences, with the most effective in reducing cell growth being the highest in modifying glucose uptake and GLUT levels.

scholarly journals Development of a novel in vitro insulin resistance model in primary human tenocytes for diabetic tendinopathy research

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e8740
Author(s):  
Hui Yee Tan ◽  
Sik Loo Tan ◽  
Seow Hui Teo ◽  
Margaret M. Roebuck ◽  
Simon P. Frostick ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Uptake ◽  
Glucose Transporter ◽  
Monolayer Culture ◽  
Immunofluorescence Staining ◽  
Type I ◽  
Expression Levels ◽  
Collagen Expression ◽  
Total Collagen ◽  
Tnf Α

Background Type 2 diabetes mellitus (T2DM) had been reported to be associated with tendinopathy. However, the underlying mechanisms of diabetic tendinopathy still remain largely to be discovered. The purpose of this study was to develop insulin resistance (IR) model on primary human tenocytes (hTeno) culture with tumour necrosis factor-alpha (TNF-α) treatment to study tenocytes homeostasis as an implication for diabetic tendinopathy. Methods hTenowere isolated from human hamstring tendon. Presence of insulin receptor beta (INSR-β) on normal tendon tissues and the hTeno monolayer culture were analyzed by immunofluorescence staining. The presence of Glucose Transporter Type 1 (GLUT1) and Glucose Transporter Type 4 (GLUT4) on the hTeno monolayer culture were also analyzed by immunofluorescence staining. Primary hTeno were treated with 0.008, 0.08, 0.8 and 8.0 µM of TNF-α, with and without insulin supplement. Outcome measures include 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl) amino]-2-deoxy-d-glucose (2-NBDG) assay to determine the glucose uptake activity; colourimetric total collagen assay to quantify the total collagen expression levels; COL-I ELISA assay to measure the COL-I expression levels and real-time qPCR to analyze the mRNA gene expressions levels of Scleraxis (SCX), Mohawk (MKX), type I collagen (COL1A1), type III collagen (COL3A1), matrix metalloproteinases (MMP)-9 and MMP-13 in hTeno when treated with TNF-α. Apoptosis assay for hTeno induced with TNF-α was conducted using Annexin-V FITC flow cytometry analysis. Results Immunofluorescence imaging showed the presence of INSR-β on the hTeno in the human Achilles tendon tissues and in the hTeno in monolayer culture. GLUT1 and GLUT4 were both positively expressed in the hTeno. TNF-α significantly reduced the insulin-mediated 2-NBDG uptake in all the tested concentrations, especially at 0.008 µM. Total collagen expression levels and COL-I expression levels in hTeno were also significantly reduced in hTeno treated with 0.008 µM of TNF-α. The SCX, MKX and COL1A1 mRNA expression levels were significantly downregulated in all TNF-α treated hTeno, whereas the COL3A1, MMP-9 and MMP-13 were significantly upregulated in the TNF–α treated cells. TNF-α progressively increased the apoptotic cells at 48 and 72 h. Conclusion At0.008 µM of TNF-α, an IR condition was induced in hTeno, supported with the significant reduction in glucose uptake, as well as significantly reduced total collagen, specifically COL-I expression levels, downregulation of candidate tenogenic markers genes (SCX and MKX), and upregulation of ECM catabolic genes (MMP-9 and MMP-13). Development of novel IR model in hTeno provides an insight on how tendon homeostasis could be affected and can be used as a tool for further discovering the effects on downstream molecular pathways, as the implication for diabetic tendinopathy.

scholarly journals Haloperidol and aripiprazole impact on the BDNF and glucocorticoid receptor levels in the rat hippocampus and prefrontal cortex: effect of the chronic mild stress

2021 ◽  
Vol 55 (3) ◽  
pp. 153-162
Author(s):  
Jana Osacka ◽  
Romana Koprdova ◽  
Andrej Tillinger ◽  
Zdenko Pirnik ◽  
Alexander Kiss
Keyword(s):  
Prefrontal Cortex ◽  
Weight Gain ◽  
Glucocorticoid Receptor ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Typical Antipsychotic ◽  
Mrna Levels ◽  
Frozen Sections ◽  
Bdnf Mrna ◽  
The Brain

Abstract Objective. Changes in the brain derived neurotrophic factor (BDNF) and glucocorticoid receptor (GR) expression in the prefrontal cortex (PFC) and hippocampus (HIP) are associated with psychiatric diseases and stress response. Chronic mild stress (CMS) may alter BDNF as well as GR levels in both the PFC and the HIP. The aim of the present study was to find out whether chronic treatment with a typical antipsychotic haloperidol (HAL) and an atypical antipsychotic aripiprazole (ARI) may modify the CMS effect on the BDNF and GR expression in the above-mentioned structures. Methods. The rats were exposed to CMS for 3 weeks and from the 7th day of CMS injected with vehicle (VEH), HAL (1 mg/kg) or ARI (10 mg/kg) for 4 weeks. BDNF and GR mRNA levels were established in the PFC and the HIP by Real Time PCR, whereas, PFC and HIP samples were obtained by punching them from 500 µm thick frozen sections. C-Fos immunoreactivity was analyzed in the PFC and the HIP on 30 µm thick paraformaldehyde fixed sections. Weight gain and corticosterone (CORT) levels were also measured. Results. The CMS and HAL suppressed the BDNF and GR mRNA levels in the PFC. In the HIP, CMS elevated BDNF mRNA levels that were suppressed by HAL and ARI treatments. The CMS decreased the c-Fos immunoreactivity in the PFC in both HAL- and ARI-treated animals. In the HIP, HAL increased the c-Fos immunoreactivity that was again diminished in animals exposed to CMS. Stressed animals gained markedly less weight until the 7th day of CMS, however, later their weight gain did not differ from the unstressed ones or was even higher in CMS+HAL group. Un-stressed HAL and ARI animals gained less weight than the VEH ones. Neither CMS nor HAL/ARI affected the plasma CORT levels. Conclusion. The present data indicate that HAL and ARI in the doses 1 mg/kg or 10 mg/kg, respectively, does not modify the effect of the CMS preconditioning on the BDNF and GR mRNA levels in the PFC or the HIP. However, HAL seems to modify the CMS effect on the HIP activation.

scholarly journals Differential Expression of HTR2A and MAOA Genes in the Prefrontal Cortex and Hypothalamus of Suicide Victims from a Mexican Population

2020 ◽  
Author(s):  
Daniel Francisco Ramos ◽  
Edna Madai Mendez ◽  
José Manuel Salas ◽  
Alma Cristina Salas ◽  
Norma Urtiz ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Differential Expression ◽  
Monoamine Oxidase A ◽  
Mexican Population ◽  
Health Concern ◽  
Expression Levels ◽  
Control Subjects ◽  
Increased Risk ◽  
Group A ◽  
The Brain

Abstract Background: Suicide is a major public health concern that has been associated with several neurobiological abnormalities, including dysfunction of the serotonin (5-HT) neurotransmission system. The serotonin 2A receptor (5-HT 2A ) and the monoamine oxidase A enzyme (MAO-A), which is responsible for degrading 5-HT, are encoded by the HTR2A and MAOA genes, respectively. These genes have been associated with several psychiatric disorders and an increased risk for suicide. Methods: Our study examined the expression levels of HTR2A and MAOA genes in the postmortem prefrontal cortex (Brodmann area 8/9) and hypothalamus (ventromedial nucleus) tissues from 15 suicide victims and 15 control subjects from a Mexican population. Gene-expression profile quantification was carried out by qPCR and determined by the method. Results: In suicide victims, the expression levels of the HTR2A gene were significantly higher in the prefrontal cortex. In contrast, the expression of the MAOA gene in the hypothalamus of the suicide victims was significantly higher than in the control subjects. When comparing adult controls against adult suicidal victims (25-59 year-old age group), a significant decrease in HTR2A expression in the hypothalamus was observed. These results were consistent regardless of age, sex, postmortem interval, or pH of brain tissue. Conclusions: The evidence suggests that the pattern of differential expression of the HTR2A and MAOA genes in the brain may be involved in suicide, providing a possible molecular basis for the brain abnormalities in suicide victims.

scholarly journals Exploring Molecular Mechanisms Involved in the Development of the Depression-Like Phenotype in Interleukin-18-Deficient Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Kyosuke Yamanishi ◽  
Masahiro Miyauchi ◽  
Keiichiro Mukai ◽  
Takuya Hashimoto ◽  
Noriko Uwa ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Molecular Mechanisms ◽  
Depressive Disorders ◽  
Psychiatric Symptoms ◽  
Neural Function ◽  
Mild Stress ◽  
Interleukin 18 ◽  
Human Brain Tissue ◽  
The Impact ◽  
The Brain

Interleukin-18 (IL-18) is an inflammatory cytokine that has been linked to energy homeostasis and psychiatric symptoms such as depression and cognitive impairment. We previously revealed that deficiency in IL-18 led to hippocampal abnormalities and resulted in depression-like symptoms. However, the impact of IL-18 deficiency on other brain regions remains to be clarified. In this study, we first sought to confirm that IL-18 expression in neural cells can be found in human brain tissue. Subsequently, we examined the expression of genes in the prefrontal cortex of Il18−/− mice and compared it with gene expression in mice subjected to a chronic mild stress model of depression. Extracted genes were further analyzed using Ingenuity® Pathway Analysis, in which 18 genes common to both the chronic mild stressed model and Il18−/− mice were identified. Of those, 16 were significantly differentially expressed between Il18+/+ and Il18−/− mice. We additionally measured protein expression of α-2-HS-glycoprotein (AHSG) and transthyretin (TTR) in serum and the brain. In the prefrontal cortex of Il18−/− mice, TTR but not AHSG was significantly decreased. Conversely, in the serum of Il18−/− mice, AHSG was significantly increased but not TTR. Therefore, our results suggest that in IL-18-deficit conditions, TTR in the brain is one of the mediators causally related to depression, and AHSG in peripheral organs is one of the regulators inducing energy imbalance. Moreover, this study suggests a possible “signpost” to clarify the molecular mechanisms commonly underlying the immune system, energy metabolism, neural function, and depressive disorders.

scholarly journals trans-Cinnamaldehyde Reverses Depressive-Like Behaviors in Chronic Unpredictable Mild Stress Rats by Inhibiting NF-κB/NLRP3 Inflammasome Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-17 ◽  
Author(s):  
Meng Wang ◽  
Shuguang Yan ◽  
Yongxue Zhou ◽  
Pei Xie
Keyword(s):  
Prefrontal Cortex ◽  
Nlrp3 Inflammasome ◽  
Active Component ◽  
Control Group ◽  
Mild Stress ◽  
Pharmacological Effects ◽  
Nf Kappa B ◽  
Treatment Of Depression ◽  
Immobility Time ◽  
Anti Inflammation

trans-Cinnamaldehyde (TCA) is the main active component extracted from Cinnamomum cassia (C. cassia), which has many pharmacological effects, such as anti-inflammation, lowering blood glucose, and improving nerve function. However, there is no report of TCA in the treatment of depression. The purpose of this study was to investigate the antidepressant-like effect of TCA and the mechanism of NF kappa B (NF-κB) pathway and NLRP3 inflammasome inhibition by TCA. We divided 40 rats into the control group, CUMS group, FLU group, and the TCA group. The activation of the NF-κB pathway and NLRP3 inflammasome in prefrontal cortex and hippocampus of rats in each group was observed. After the treatments with FLU and TCA, the sucrose consumptions in rats increased significantly and the immobility time in forced swimming was decreased significantly compared to the CUMS group. The expression of TLR4, NF-κB-1, p-p65, TNF-α, NLRP3, ASC, caspase-1, IL-1β, and IL-18 proteins in prefrontal cortex and hippocampus was decreased, and the expression of IL-1β, IL-18, and TNF-α in serum was downregulated compared to the CUMS group. Similar to FLU, TCA reverses the depression-like behaviors in rats, which indicates that TCA has a significant antidepressant-like effect. The mechanism of the antidepressant property of TCA might be that it inhibits the activation of the NF-κB pathway and NLRP3 inflammasome in the prefrontal cortex and hippocampus of CUMS rats.

scholarly journals Scavenging ROS Decreases Amyloid-beta Levels via Activation of PI3K/Akt/GLUT1 pathway in N2a/APP695swe Cells

2021 ◽  
Author(s):  
Yan Peng ◽  
Li Zhang ◽  
Fanlin Zhou ◽  
Yangyang Wang ◽  
Shijie Li ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Glucose Transporter ◽  
Akt Pathway ◽  
Glucose Transporter 1 ◽  
Abnormal Glucose Metabolism ◽  
Glut1 Expression ◽  
Ros Scavenger ◽  
Underlying Mechanisms ◽  
The Brain

Abstract Dysregulated glucose metabolism in the brain is considered to be the underlying cause of Alzheimer's disease (AD). Abnormal glucose metabolism in AD is associated with decreased glucose transporter 1 (GLUT1) and GLUT3 in the brain, but the underlying mechanisms remains unclear. Here, we reported that GLUT1 expression was decreased in N2a/APP695swe cells and GLUT3 expression was not significantly changed. Flow Cytometry analysis showed a significant increase of intracellular ROS content in N2a/APP695swe cells and GLUT1 expression was upregulated after treatment with the ROS scavenger N-acetyl-L-Cysteine (NAC). Cellular glucose uptake and ATP levels were reduced following decreased GLUT1 expression and increased after upregulating GLUT1. Western blot analyses showed that phosphorylation of PI3K/Akt pathway decreased in N2a/APP695swe cells. Aβ levels decreased after upregulation of GLUT1 expression and increased after downregulation of GLUT1. After NAC treatment, PI3K/Akt pathway phosphorylation levels and GLUT1 expression were upregulated, glucose uptake and ATP contents were increased, and Aβ levels were decreased. After adding PI3K/Akt pathway inhibitor LY29004, GLUT1 expression was reduced and Aβ levels were increased. Besides, the increased glucose uptake and ATP contents by the Akt activator SC79 were hindered with the GLUT1 inhibitor WZB117. Aβ levels decreased after SC79 treatment and increased after WZB117 treatment. Overall, our data suggest that ROS reduced GLUT1 expression by inhibiting PI3K/Akt pathway activity resulting in impaired glucose metabolism and scavenging ROS prevents Aβ via activation of PI3K/Akt/GLUT1 pathway in N2a/APP695swe cells.

scholarly journals GLUT2-Mediated Glucose Uptake and Availability Are Required for Embryonic Brain Development in Zebrafish

2014 ◽  
Vol 35 (1) ◽  
pp. 74-85 ◽  
Author(s):  
Rubén Marín-Juez ◽  
Mireia Rovira ◽  
Diego Crespo ◽  
Michiel van der Vaart ◽  
Herman P Spaink ◽  
...  
Keyword(s):  
Brain Development ◽  
Glucose Uptake ◽  
Neural Progenitor Cells ◽  
Glucose Transporter ◽  
Glucose Sensing ◽  
Glucose Transporter 2 ◽  
Glut2 Gene ◽  
Glucose Dynamics ◽  
The Brain

Glucose transporter 2 (GLUT2; gene name SLC2A2) has a key role in the regulation of glucose dynamics in organs central to metabolism. Although GLUT2 has been studied in the context of its participation in peripheral and central glucose sensing, its role in the brain is not well understood. To decipher the role of GLUT2 in brain development, we knocked down slc2a2 ( glut2), the functional ortholog of human GLUT2, in zebrafish. Abrogation of glut2 led to defective brain organogenesis, reduced glucose uptake and increased programmed cell death in the brain. Coinciding with the observed localization of glut2 expression in the zebrafish hindbrain, glut2 deficiency affected the development of neural progenitor cells expressing the proneural genes atoh1b and ptf1a but not those expressing neurod. Specificity of the morphant phenotype was demonstrated by the restoration of brain organogenesis, whole-embryo glucose uptake, brain apoptosis, and expression of proneural markers in rescue experiments. These results indicate that glut2 has an essential role during brain development by facilitating the uptake and availability of glucose and support the involvement of glut2 in brain glucose sensing.

scholarly journals The Rho/Rac Guanine Nucleotide Exchange Factor Vav1 Regulates Hif-1α and Glut-1 Expression and Glucose Uptake in the Brain

2020 ◽  
Vol 21 (4) ◽  
pp. 1341
Author(s):  
Jaewoo Hong ◽  
Yurim Kim ◽  
Sudhirkumar Yanpallewar ◽  
P. Charles Lin
Keyword(s):  
Endothelial Cells ◽  
Glucose Uptake ◽  
Glucose Transporter ◽  
Guanine Nucleotide Exchange Factor ◽  
Guanine Nucleotide ◽  
Nucleotide Exchange ◽  
Glut 1 ◽  
Guanine Nucleotide Exchange ◽  
Nucleotide Exchange Factor ◽  
The Brain

Vav1 is a Rho/Rac (Ras-related C3 botulinum toxin substrate) guanine nucleotide exchange factor expressed in hematopoietic and endothelial cells that are involved in a wide range of cellular functions. It is also stabilized under hypoxic conditions when it regulates the accumulation of the transcription factor HIF (Hypoxia Inducible Factor)-1α, which activates the transcription of target genes to orchestrate a cellular response to low oxygen. One of the genes induced by HIF-1α is GLUT (Glucose Transporter)-1, which is the major glucose transporter expressed in vessels that supply energy to the brain. Here, we identify a role for Vav1 in providing glucose to the brain. We found that Vav1 deficiency downregulates HIF-1α and GLUT-1 levels in endothelial cells, including blood-brain barrier cells. This downregulation of GLUT-1, in turn, reduced glucose uptake to endothelial cells both in vitro and in vivo, and reduced glucose levels in the brain. Furthermore, endothelial cell-specific Vav1 knock-out in mice, which caused glucose uptake deficiency, also led to a learning delay in fear conditioning experiments. Our results suggest that Vav1 promotes learning by activating HIF-1α and GLUT-1 and thereby distributing glucose to the brain. We further demonstrate the importance of glucose transport by endothelial cells in brain functioning and reveal a potential new axis for targeting GLUT-1 deficiency syndromes and other related brain diseases.

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