scholarly journals Reciprocal change in Glucose metabolism of Cancer and Immune Cells mediated by different Glucose Transporters predicts Immunotherapy response

Theranostics ◽  
2020 ◽  
Vol 10 (21) ◽  
pp. 9579-9590
Author(s):  
Kwon Joong Na ◽  
Hongyoon Choi ◽  
Ho Rim Oh ◽  
Yoon Ho Kim ◽  
Sae Bom Lee ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Immune Cells ◽  
Glucose Transporters ◽  
Reciprocal Change

scholarly journals LncRNA HOTAIR regulates glucose transporter Glut1 expression and glucose uptake in macrophages during inflammation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Monira Obaid ◽  
S. M. Nashir Udden ◽  
Prasanna Alluri ◽  
Subhrangsu S. Mandal
Keyword(s):  
Immune Response ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Immune Cells ◽  
Glucose Transporter ◽  
Energy Needs ◽  
Glut1 Expression ◽  
Lncrna Hotair ◽  
Upstream Regulators ◽  
Glucose Transporter Glut1

AbstractInflammation plays central roles in the immune response. Inflammatory response normally requires higher energy and therefore is associated with glucose metabolism. Our recent study demonstrates that lncRNA HOTAIR plays key roles in NF-kB activation, cytokine expression, and inflammation. Here, we investigated if HOTAIR plays any role in the regulation of glucose metabolism in immune cells during inflammation. Our results demonstrate that LPS-induced inflammation induces the expression of glucose transporter isoform 1 (Glut1) which controls the glucose uptake in macrophages. LPS-induced Glut1 expression is regulated via NF-kB activation. Importantly, siRNA-mediated knockdown of HOTAIR suppressed the LPS-induced expression of Glut1 suggesting key roles of HOTAIR in LPS-induced Glut1 expression in macrophage. HOTAIR induces NF-kB activation, which in turn increases Glut1 expression in response to LPS. We also found that HOTAIR regulates glucose uptake in macrophages during LPS-induced inflammation and its knockdown decreases LPS-induced increased glucose uptake. HOTAIR also regulates other upstream regulators of glucose metabolism such as PTEN and HIF1α, suggesting its multimodal functions in glucose metabolism. Overall, our study demonstrated that lncRNA HOTAIR plays key roles in LPS-induced Glut1 expression and glucose uptake by activating NF-kB and hence HOTAIR regulates metabolic programming in immune cells potentially to meet the energy needs during the immune response.

scholarly journals Glucose Metabolism and Glucose Transporters in Breast Cancer

2021 ◽  
Vol 9 ◽  
Author(s):  
Eunah Shin ◽  
Ja Seung Koo
Keyword(s):  
Breast Cancer ◽  
Glucose Metabolism ◽  
Stromal Cells ◽  
Warburg Effect ◽  
Molecular Subtype ◽  
Cell Metabolism ◽  
Treatment Strategies ◽  
Glucose Transporters ◽  
Pentose Phosphate ◽  
Cancer Prognosis

Breast cancer is the most common malignancy in women worldwide and is associated with high mortality rates despite the continuously advancing treatment strategies. Glucose is essential for cancer cell metabolism owing to the Warburg effect. During the process of glucose metabolism, various glycolytic metabolites, such as serine and glycine metabolites, are produced and other metabolic pathways, such as the pentose phosphate pathway (PPP), are associated with the process. Glucose is transported into the cell by glucose transporters, such as GLUT. Breast cancer shows high expressions of glucose metabolism-related enzymes and GLUT, which are also related to breast cancer prognosis. Triple negative breast cancer (TNBC), which is a high-grade breast cancer, is especially dependent on glucose metabolism. Breast cancer also harbors various stromal cells such as cancer-associated fibroblasts and immune cells as tumor microenvironment, and there exists a metabolic interaction between these stromal cells and breast cancer cells as explained by the reverse Warburg effect. Breast cancer is heterogeneous, and, consequently, its metabolic status is also diverse, which is especially affected by the molecular subtype, progression stage, and metastatic site. In this review, we will focus on glucose metabolism and glucose transporters in breast cancer, and we will additionally discuss their potential applications as cancer imaging tracers and treatment targets.

scholarly journals Depletion of mitochondrial DNA alters glucose metabolism in SK-Hep1 cells

2001 ◽  
Vol 280 (6) ◽  
pp. E1007-E1014 ◽  
Author(s):  
Kyu-Sang Park ◽  
Kyung-Jay Nam ◽  
Jun-Woo Kim ◽  
Youn-Bok Lee ◽  
Chang-Yeop Han ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Glucose Metabolism ◽  
Nuclear Dna ◽  
Glucose Transporters ◽  
Diabetic Patients ◽  
Human Hepatoma Cells ◽  
Metabolizing Enzymes ◽  
Atp Production ◽  
Protein Levels

Maternally inherited mitochondrial DNA (mtDNA) has been suggested to be a genetic factor for diabetes. Reports have shown a decrease of mtDNA content in tissues of diabetic patients. We investigated the effects of mtDNA depletion on glucose metabolism by use of ρ0 SK-Hep1 human hepatoma cells, whose mtDNA was depleted by long-term exposure to ethidium bromide. The ρ0 cells failed to hyperpolarize mitochondrial membrane potential in response to glucose stimulation. Intracellular ATP content, glucose-stimulated ATP production, glucose uptake, steady-state mRNA and protein levels of glucose transporters, and cellular activities of glucose-metabolizing enzymes were decreased in ρ0 cells compared with parental ρ+ cells. Our results suggest that the quantitative reduction of mtDNA may suppress the expression of nuclear DNA-encoded glucose transporters and enzymes of glucose metabolism. Thus this may lead to diabetic status, such as decreased ATP production and glucose utilization.

Insight into the Glucose Metabolism of Immune Cells in Sepsis

2017 ◽  
Vol 4 (1) ◽  
pp. 38-44 ◽  
Author(s):  
Xu Liu ◽  
Shui-Jing Wu ◽  
Xiang-Ming Fang
Keyword(s):  
Glucose Metabolism ◽  
Immune Cells ◽  
Insight Into

scholarly journals Glucose metabolism pattern of peripheral blood immune cells in myasthenia gravis patients

2020 ◽  
Vol 8 (9) ◽  
pp. 577-577
Author(s):  
Zhibin Li ◽  
Yuyao Peng ◽  
Yi Li ◽  
Ran Zhou ◽  
Di Chen ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Myasthenia Gravis ◽  
Immune Cells ◽  
Peripheral Blood

scholarly journals Glucose transporters in Alzheimer's disease

BJPsych Open ◽  
2021 ◽  
Vol 7 (S1) ◽  
pp. S265-S266
Author(s):  
Natalia Kyrtata ◽  
Ben Dickie ◽  
Hedley Emsley ◽  
Laura Parkes
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glucose Metabolism ◽  
Animal Models ◽  
Glucose Transport ◽  
Glucose Transporters ◽  
Human Studies ◽  
Glucose Regulation ◽  
Randomised Control Trial ◽  
The Brain

BackgroundPhysiological brain function depends on tight glucose regulation, including transport and phosphorylation, the first step in its metabolism. Impaired glucose regulation is increasingly implicated in the pathophysiology of Alzheimer's disease (AD). Glucose hypometabolism in AD may be at least partly due to impaired glucose transport at the blood-brain barrier (BBB). Glucose transporters (GLUTs) are an integral component of the BBB. There is evidence of a significant reduction in vascular and non-vascular forms of GLUT1 and GLUT3 in AD brains compared to age-matched controls. Glucose transport, as well as phosphorylation, appears to be a rate limiting step for glucose metabolism in the brain. We have reviewed the literature on glucose transport abnormalities in AD and the effect such abnormalities have on the brain.MethodPublished literature between 1st January 1946 and 1st November 2019 was identified using EMBASE and MEDLINE databases and titles and abstracts were scanned. Human studies (autopsy and imaging) and data from animal models were included while reviews, letters and cellular or molecular studies were excluded from the search.ResultAutopsy studies in AD patients show significant reductions in GLUT3 in areas of the brain closely associated with AD pathology. Patients with AD and diabetes showed greater reductions of GLUT1 and GLUT3. A longitudinal study showed significant reductions in GLUT3 levels which correlated with greater amyloid-β (Aβ) and neurofibrillary tangle pathological burden in participants with AD pathology at post-mortem but without evidence of cognitive dysfunction in their lifetime. Some studies showed increased GLUT1, with others showing reduced GLUT1, levels in AD brain. A newly recognised GLUT12 appears to be increased in AD. Animal studies showed similar results with GLUT1 and GLUT3 knockout animal models exhibiting AD pathology, while overexpression of GLUT1 or treatment with metformin decreased Aβ toxicity in a Drosophila model of AD. GLUT2 levels were increased in both human AD brain and in an animal model of AD. Imaging studies using fluorodeoxyglucose [18F]FDG with positron emission tomography (FDG-PET) in AD subjects show reductions in glucose transport and glucose metabolism in areas most affected in AD. A small randomised control trial showed anti-diabetic medications improved the glucose transport in AD subjects.ConclusionGLUTs play a significant role in AD pathology with evidence suggesting that GLUT3 reductions may precede the onset of clinical symptoms, while GLUT2 and GLUT12 may have a compensatory role. Repurposing anti-diabetic drugs shows promising results in both animal and human studies of AD.

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