Relevant bibliographies by topics / Glucose-mediated

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Glucose-mediated'

Author: Grafiati
Published: 6 September 2023

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Journal articles on the topic "Glucose-mediated"

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Kagotho, Elizabeth. "Insulin-Mediated Glucose Metabolism: An Atherogenic Lipid Profile of Fructose Consumption." Endocrinology and Disorders 2, no. 2 (February 27, 2018): 01–02. http://dx.doi.org/10.31579/2640-1045/096.

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Our laboratory has investigated two hypotheses regarding the effects of fructose consumption: 1) The endocrine effects of fructose consumption favor a positive energy balance, and 2) Fructose consumption promotes the development of an atherogenic lipid profile. In previous short- and long-term studies, we demonstrated that consumption of fructose-sweetened beverages with 3 meals results in lower 24-hour plasma concentrations of glucose, insulin, and leptin in humans compared with consumption of glucose-sweetened beverages. We have also tested whether prolonged consumption of high-fructose diets could lead to increased caloric intake or decreased energy expenditure, thereby contributing to weight gain and obesity. Results from a study conducted in rhesus monkeys produced equivocal results. Carefully controlled and adequately powered long-term studies are needed to address these hypotheses. In both short- and long-term studies we demonstrated that consumption of fructose-sweetened beverages substantially increases postprandial triacylglycerol concentrations compared with glucose-sweetened beverages. In the long-term studies, apolipoproteinB concentrations were also increased in subjects consuming fructose, but not those consuming glucose. Data from a short-term study comparing consumption of beverages sweetened with fructose, glucose, high fructose corn syrup (HFCS) and sucrose, suggest that HFCS and sucrose increase postprandial triacylglycerol to an extent comparable to that induced by 100% fructose alone. Increased consumption of fructose-sweetened beverages along with increased prevalence of obesity, metabolic syndrome, and type 2 diabetes underscore the importance of investigating the metabolic consequences fructose consumption in carefully controlled experiments.
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Kagotho, Elizabeth. "Insulin-Mediated Glucose Metabolism: An Atherogenic Lipid Profile of Fructose Consumption." Endocrinology and Disorders 2, no. 2 (February 15, 2018): 01–02. http://dx.doi.org/10.31579/2640-1045/021.

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Seaquist, E. R., K. Pyzdrowski, A. Moran, A. U. Teuscher, and R. P. Robertson. "Insulin-mediated and glucose-mediated glucose uptake following hemipancreatectomy in healthy human donors." Diabetologia 37, no. 10 (September 1, 1994): 1036–43. http://dx.doi.org/10.1007/s001250050214.

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Seaquist, E. R., K. Pyzdrowski, A. Moran, A. U. Teuscher, and R. P. Robertson. "Insulin-mediated and glucose-mediated glucose uptake following hemipancreatectomy in healthy human donors." Diabetologia 37, no. 10 (October 1994): 1036–43. http://dx.doi.org/10.1007/bf00400467.

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Fink, R. I., P. Wallace, and J. M. Olefsky. "Effects of aging on glucose-mediated glucose disposal and glucose transport." Journal of Clinical Investigation 77, no. 6 (June 1, 1986): 2034–41. http://dx.doi.org/10.1172/jci112533.

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Mohsin, Mahmoud A., Yousef Haik, and Tahir Abdulrehman. "Glucose-Mediated Insulin Release Carrier." Polymer Science, Series A 60, no. 5 (September 2018): 618–27. http://dx.doi.org/10.1134/s0965545x18050097.

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Atanasov, P., A. Kaisheva, S. Gamburzev, I. Iliev, and S. Bobrin. "Nickelocene-mediated glucose oxidase electrode." Electroanalysis 5, no. 1 (January 1993): 91–97. http://dx.doi.org/10.1002/elan.1140050114.

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Patolsky, Fernando, Guoliang Tao, Eugenii Katz, and Itamar Willner. "C60-mediated bioelectrocatalyzed oxidation of glucose with glucose oxidase." Journal of Electroanalytical Chemistry 454, no. 1-2 (August 1998): 9–13. http://dx.doi.org/10.1016/s0022-0728(98)00257-5.

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Regittnig, W., Z. Trajanoski, G. Brunner, H. J. Leis, T. Pieber, and P. Wach. "Glucose-Mediated Glucose Dynamics after Intravenous Glucose Injection in Insulin-Dependent Diabetic Subjects." IFAC Proceedings Volumes 30, no. 2 (March 1997): 85–87. http://dx.doi.org/10.1016/s1474-6670(17)44547-2.

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Jeon, Won-Yong, Young-Bong Choi, Bo-Hee Lee, Ho-Jin Jo, Soo-Yeon Jeon, Chang-Jun Lee, and Hyug-Han Kim. "Glucose detection via Ru-mediated catalytic reaction of glucose dehydrogenase." Advanced Materials Letters 9, no. 3 (March 2, 2018): 220–24. http://dx.doi.org/10.5185/amlett.2018.1947.

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Dissertations / Theses on the topic "Glucose-mediated"

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Lloyd, Kenneth P. "Understanding Human Erythrocyte Glucose Transporter (GLUT1) Mediated Glucose Transport Phenomena Through Structural Analysis." eScholarship@UMMS, 2018. https://escholarship.umassmed.edu/gsbs_diss/962.

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GLUT1-mediated, facilitated sugar transport is proposed to be an example of transport by a carrier that alternately presents exofacial (e2) and endofacial (e1) substrate binding sites, commonly referred to as the alternating access carrier model. This hypothesis is incompatible with observations of co-existent exo- and endofacial ligand binding sites, transport allostery, and e1 ligand (e.g. cytochalasin B) induced GLUT1 sugar occlusion. The fixed-site carrier model proposes co-existent, interacting e2 and e1 ligand binding sites but involves sugar translocation by geminate exchange through internal cavities. Demonstrations of membrane-resident dimeric and tetrameric GLUT1 and of e2, e1 and occluded GLUT conformations in GLUT crystals of monodisperse, detergent-solubilized proteins suggest a third model. Here, GLUT1 is an alternating access carrier but the transporter complex is a dimer of GLUT1 dimers, in which subunit interactions produce two e2 and two e1 conformers at any instant. The crystallographic structures in different conformations can be utilized to further understand the transport cycle, ligand binding behavior and complex kinetics observed in GLUT1. Specifically, the GLUT1 crystal structure and homology models based upon related major facilitator superfamily proteins were used in this study, to understand inhibitor binding, ligand binding induced GLUT1 transport allostery and the existence of helix packing/oligomerization motifs and glycine induced flexibility. These studies suggest that GLUT1 functions as an oligomeric allosteric carrier where cis-allostery is an intramolecular behavior and trans-allostery is an intermolecular behavior. Additionally, mutations of a dynamic glycine affect the turnover of the transporter while mutations to helix packing motifs affect affinity.
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Ojelabi, Ogooluwa A. "Small Molecule Modulation of GLUT1-Mediated Glucose Transport." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/950.

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The glucose transport protein, GLUT1, is highly expressed in rapidly proliferating cells, including cancer cells, while decreased GLUT1 levels are found in diseases such as GLUT1 deficiency syndrome and Alzheimer’s. There is increased interest in developing GLUT1 inhibitors as novel anticancer therapeutics, and the discovery of compounds that directly stimulate GLUT1 function. This work investigates how small molecules stimulate and/or inhibit GLUT1-mediated glucose transport, either directly or through the AMPK pathway. Using sugar transport assays and docking analyses to explore Ligand–GLUT1 interactions and specificity of binding, we show that: 1) Ligands inhibit GLUT1 by competing with glucose for binding to the exofacial or endofacial sugar binding sites; 2) Subsaturating inhibitor concentrations stimulate sugar uptake; 3) Ligands inhibit GLUT1–, GLUT3– and GLUT4–mediated sugar uptake in HEK293 cells; and 4) Inclusion of a benzonitrile head group on endofacial GLUT1 inhibitors confers greater inhibitory potency. Furthermore, we investigated AMPK-regulated GLUT1 trafficking in cultured blood-brain barrier endothelial cells, and show that inhibition of GLUT1 internalization is not responsible for increased cell surface levels of GLUT1 observed with AMPK activation in these cells. This study provides a framework for screening candidate GLUT1 inhibitors for specificity, and for optimizing drug design and delivery. Our data on transport stimulation at low inhibitor concentrations support the idea that GLUT1 functions as a cooperative oligomer of allosteric alternating access subunits.
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Brenner, Corinne. "Immune-mediated regulation of glucose uptake in human adipocytes." Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/7126.

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I have investigated the potential role of Toll-Like Receptors (TLRs) in mediating adipose inflammation in obesity. TLRs are a family of pattern recognition receptors that play a key role in host defence and are also implicated in chronic inflammatory disorders. The finding that TLR4-deficient mice are protected against obesity-induced diabetes led me to hypothesise that TLR expression on adipocytes could play a role in obesity-induced adipose inflammation and metabolic dysfunction. The first chapter investigates the expression and function of TLRs in in vitro differentiated human subcutaneous adipocytes. I found that stimulation with ligands for TLR2, TLR3 and TLR4 but not the other TLRs, induces the expression of pro-inflammatory cytokines. I also explored the use of the TLR adapter molecules MyD88, Mal and TRIF by different TLRs. The second chapter examines whether TLR activation in adipocytes has an effect on glucose uptake. I established a 3H-2-deoxy-D-glucose (2DOG) uptake assay which led to an interesting yet unexpected observation: Stimulation with TLR3 and TLR4 ligands led to a decrease in insulin-stimulated glucose uptake but at the same time, insulin-independent glucose uptake was increased. I showed that these observations are at least partly due to altered expression of different glucose transporter (GLUT) isoforms. As the effects were seen only after prolonged TLR stimulation, I speculated that this was mediated via a secondary secreted factor. The third chapter is based on a cytokine and adipokine array, which I performed to identify cytokines that may be responsible for the effects described in Chapter 2. The secretion of several cytokines/chemokines with diverse pro-inflammatory functions was observed following stimulation with TLR3 and TLR4 ligands. The contribution of some of these factors to altered glucose handling was investigated. Whilst a contribution for ENA-78 was ruled out, I present evidence that IL-1 can contribute to this.
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Harper, Alice C. "Modified Electrodes for Amperometric Determination of Glucose and Glutamate Using Mediated Electron Transport." Diss., Virginia Tech, 2005. http://hdl.handle.net/10919/28098.

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The main goal of this research was to develop an easy to prepare and sensitive biosensor that would be able to detect glutamate in solution using ionic self-assembly methods. This was accomplished by preparing an ionically-self-assembled monolayer that included an electron transport mediator and an enzyme that would generate a current proportional to the concentration of analytes in solution. Biosensors were produced for the detection of glucose and glutamate. Ferrocene poly(allylamine) (FePAA) was assembled on negatively charged self-assembled monolayer and shown to be electrostatically bound by cyclic voltammetry. Model films were made of FePAA and poly(styrenesulfonate) to determine if multilayer films could be assembled using electrostatic assembly. These experiments demonstrated that 7 bilayers is the maximum number of bilayers oxidizable by the heterogeneous reaction at the electrode surface. ISAMs were then assembled on a 2 mm gold electrode and on a gold fiber microelectrode using FePAA and glucose oxidase. Using cyclic voltammetry, these ISAMs were shown to be able to oxidize glucose in solution. The LOD was determined to be lower for the microelectrode than for the 2 mm gold electrode, which was expected, while both compared well to the literature. The Km? were found to be smaller than other glucose biosensors while the Icat increased with increasing number of bilayers. This demonstrated that the GluOx is making good electrical contact with the layer below. These glucose oxidase ISAMs, however, do not exhibit structural stability in flow-injection experiments. As a solution to the ISAM modified electrodes degrading in the flowing system, a covalently modified surface was developed. Using cyclic voltammetry, these covalently modified surfaces were shown to be able to oxidize glucose in solution. The LOD of the covalently modified 2 mm gold electrode was calculated to be lower than the 2 mm ISAM modified gold electrode, due to the fast heterogeneous kinetics on the covalently modified electrode surface. The Km? and Icat for the covalently modified 2 mm gold electrode were found to be the similar to the 2 mm ISAM modified gold electrode indicating that the covalently modified electrodes will be a suitable replacement. The covalently modified surfaces exhibit excellent structural stability and detect much lower glucose amounts in flow-injection experiments. ISAMs were subsequently assembled on gold fiber microelectrodes using FePAA and glutamate oxidase. Glutamate was able to be detected in solution at biologically significantly quantities using cyclic voltammetry. The Km? was shown to be comparable to literature values and Icat was shown to increase with increasing number of bilayers. These results demonstrate that an ISAM constructed using FePAA/GlutOx is a feasible way to detect glutamate in a system.
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Dwyer, Peter M. "Effects of daipose-specific glucose transporter type 4 expression on glucose homeostasis mediated through alterations in adipose tissue composition." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12356.

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Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
Objective: Rates of obesity are rising in the U.S. and on a global scale. With this increasing incidence of obesity we are seeing an accompanying rise in the pathologies associated with type II diabetes mellitus (DMII) such as altered insulin sensitivity and glucose homeostasis. The notion of the adipocyte as a biologically dynamic cell is becoming more prevalent and recent evidence implicates the adipocyte as a key regulator in the onset of the aforementioned pathologies. The aim of this study is to further elucidate how changes in the expression of glucose transporter type 4 (GLUT4) in adipocytes may alter adipose tissue function and biology, specifically, if and how these alterations may affect downstream metabolic functions such as glucose uptake. Methods: Male and female adipose-specific GLUT4 overexpressor (AG40x) mice along with wild type (WT) littermates were monitored for changes in weight, body fat percentage, glucose tolerance and adipocyte metabolism over a period of 10-18 weeks. Additional cohorts of the transgenic and WT animals were also treated with a high energy diet to exacerbate any potential differences. Results: AG40x animals on a balanced diet showed high glucose clearance rates compared to WT animals; however, the high energy diet impaired glucose clearance for the AG40x animals. Overexpression of GLUT4 in adipose promotes increased weight gain and fat deposition but does not significantly alter adipose tissue composition compared to the WT balanced diet animals. Conclusion: Although overexpression of GLUT4 in adipose tissue appears to bring about undesired effects of weight gain, these animals were protected from adverse weight gain when challenged with a high energy diet. In both transgenic study groups, fat percentages are increased although adipose composition tissue was no significantly altered as seen in WT high-energy diet animals. This may contribute to the improved glucose clearance profiles seen in this particular model suggesting a potential therapeutic target for those who are high risk for DMII.
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Stone, Claire Gemma. "Antioxidants and trace elements : effect on mediated electron transfer in glucose biosensors." Thesis, University of Surrey, 2006. http://epubs.surrey.ac.uk/763/.

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Püschel, Franziska. "Cell death and cytokine-mediated inflammatory responses to glucose deprivation in cancer cells." Doctoral thesis, Universitat de Barcelona, 2019. http://hdl.handle.net/10803/667909.

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Metabolic alterations in cancer cells are primarily caused by oncogenic mutations and cancer cells are more dependent on glucose compared to non-transformed tissue. Targeting the cancer metabolism opens up a new strategy for anti-cancer therapy. In order to make drugs more efficient and applicable in the clinic, it is necessary to fully investigate the cancer cell metabolism, especially of how cancer cells die upon glucose deprivation and more importantly, the consequences on the surrounding tissue when modifying or interfering with the metabolism. The unfolded protein response (UPR) is an intracellular stress response which is induced upon glucose deprivation. The activation of the three branches of the UPR facilitates pro-survival responses, however, chronic exposure to intra- or extracellular stress results in a switch towards a pro-death UPR response. The UPR is also described to be involved in pro-inflammatory responses due to the induction of cytokines and chemokines in several cell lines. Therefore, the release of cytokines upon glucose deprivation could facilitate the infiltration or exclusion of immune cells. We hypothesized that cancer cells die in an UPR dependent manner and that cancer cells release inflammatory cytokines upon glucose deprivation, which promote the infiltration of immune cells. We found that HeLa cells exposed to glucose deprivation, died in a TRAIL receptor 1 (DR4) and 2 (DR5) dependent manner, which was mediated by the activation transcription factor 4 (ATF4). Furthermore, we found the release of pro-tumorigenic cytokines such as interleukin-8 (IL-8), interleukin-6 (IL-6) and the leukemia inhibitory factor (LIF) from glucose deprived cancer cells as well as upon treatment with anti-metabolic drugs. We found that IL 6 and IL-8 but not LIF were regulated by ATF4 and p65 upon glucose deprivation. Moreover, the conditioned media of glucose deprived A549 promoted the migration of macrophage-like THP-1 cells as well as primary B cells and neutrophils isolated from human blood. These findings are important, since interfering with the cancer metabolism by using anti metabolic drugs could suppress the anti-tumorigenic effect of these drugs by promote pro-tumorigenic responses.
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GRIMOLIZZI, FRANCO. "Neutrophils alter placental glucose metabolism in gestational diabetes mellitus via neutrophil elastase mediated IRS1 degradation." Doctoral thesis, Università Politecnica delle Marche, 2017. http://hdl.handle.net/11566/245194.

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La gravidanza è da considerarsi una condizione pro-inflammatoria dove si osserva un’attivazione dei neutrofili circolanti. Con l'avanzare della gravidanza la concentrazione nel sangue di nucleosomi e mieloperossidasi aumenta e riflette la produzione delle trappole extracellulari dei neutrofili (NETs). Abbiamo dimostrato che in corso di diabete mellito gestazionale (GDM) tale produzione è aumentata in confronto ad una gravidanza fisiologica. Elevati livelli di glucosio e TNF-a, segni tipici presenti in corso di GDM, in vitro agiscono in modo sinergico e sono in grado di pre-attivare i neutrofili ed indurre il rilascio delle NETs. Abbiamo ipotizzato che, lo stato di iperattivazione osservato a livello sistemico possa essere associato ad una aumentata attività leucocitaria a livello placentare. A sostegno della nostra ipotesi, si osserva nei villi coriali isolati da placente GDM un’aumentata infiltrazione di PMNs pro-NETotici in associazione ad un accumulo della neutrofili elastasi (NE). Per valutare un possibile effetto pro-infiammatorio del glucosio a livello placentare, abbiamo incubato cellule di trofoblasto (BeWo) in presenza di un’elevata concentrazione di glucosio e successivamente valutato la produzione di TNF-a. È stato interessante rilevare un aumento nel rilascio di TNF- a tale da indurre un effetto pro-NETotico sui PMN con consequente rilascio della NE. Da recenti ricerche è emerso come in corso di diabete e tumore la NE possa essere internalizzata dalle cellule ed alterare la trasduzione del segnale insulinico attraverso la degradazione del substrato 1 del recettore insulinico (IRS1). Esperimenti in vitro hanno dimostrato che in presenza della NE si osserva una riduzione di IRS1 nelle cellule BeWo ed una diminuzione dell’internalizzazione del glucosio. Poichè l’espressione di IRS1 risulta ridotta nelle placente GDM é verosimile ipotizzare che la massiva presenza di NE ne può essere la causa. In conclusione, i nostri dati suggeriscono che in corso di GDM si verifica un’elevata produzione di NETs ed una massiva infiltrazione di pro-NETotici PMN nella placenta. Queste scoperte dimostrano come la NETosi abbia una significativa utilità diagnostica in corso di GDM e la NE un nuovo potenziale bersaglio terapeutico.
Human pregnancy is associated with a mild pro-inflammatory state characterized by activation of circulatory neutrophils (PMNs). Skewing of PMNs responses toward to neutrophil extracellular traps generation (NETs) is reflected in an increased of circulating nucleosomes and myeloperoxidase with advancing gestational age. Our data indicated that this pro-NETotic profile is enhanced in women with gestational diabetes mellitus (GDM). Maternal hyperglycemia and increased levels of TNF-a are a hallmark of GDM and we show a synergistic effect of both factors on the priming and release of NETs. Moreover, we hypothesized that systemic activation was associated with activated PMN in placenta. Indeed, we observed a massive infiltration of pro-NETotic PMNs and neutrophil elastase (NE) accumulation along chorionic villi of GDM placentas. To further explore whether hyperglycemia predisposes to exaggerated inflammatory response in placenta we incubated trophoblast BeWo cells in high glucose conditions and we next tested the TNF-a production capacity. Interestingly, TNF-a level was incresed and exert a pro-NETotic effect on PMN with consequent NE release. Recent studies in cancer tissues and diabetes models have described that released NE induce profound changes in the surrounding cells, altering the signal transducing cascade and promoting insulin resistance via degradation of insulin receptor substrate 1 (IRS1). Our in-vitro data indicate that addition of NE to trophoblast cell line BeWo causes degradation of IRS1 with consequent glucose uptake impairment. IRS1 is reduced in GDM placentas when compared to control placentas, suggesting that the presence of NE might be the causal factor. Taken together, our data showed that GDM is characterized by excessive NET formation and by a massive influx of pro-NETotic PMN into placentas. These findings underline the competence of NETs as a highly relevant diagnostic biomarker for GDM and NE as a new potential therapeutic target.
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Bahari, Meisam. "Use of Viologens in Mediated Glucose Fuel Cells and in Aqueous Redox Flow Batteries to Improve Performance." BYU ScholarsArchive, 2020. https://scholarsarchive.byu.edu/etd/8681.

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This dissertation presents my efforts to use viologens to improve the performance of glucose fuel cells and aqueous redox flow batteries. These two electrochemical systems have the potential to efficiently exploit renewable sources of energy. The contributions and significance of this work are briefly described below. Glucose Fuel cells. For glucose fuel cells, viologens were adopted as an electron mediator to facilitate the transfer of electrons from glucose to electrodes for power generation. Use of a mediator circumvents the need for precious metal electrodes to catalyze glucose oxidation. Both the oxidation efficiency and rate of glucose oxidation are important to the viability of glucose fuel cells. Oxidation efficiency is defined as the extent to which the carbons of a carbohydrate (glucose for instance) are oxidized relative to full oxidation to carbon dioxide. The efficiency measured in this study depended on the initial molar ratio of viologen to glucose and also on the rate of the regeneration of the mediator. The maximum conversion efficiency observed was ~22%, which is about three times larger than the values observed for precious-metal-based fuel cells. Rate performance is another important aspect of a glucose fuel cell. Detailed simulations demonstrated that rate performance of viologen-mediated cells was limited principally by mass transfer. The maximum obtainable current density was ~200 mA/cm2, which is significantly higher than the rates available from biological fuel cells and comparable to the values observed for precious-metal-based fuel cells. Viologen-mediated fuel cells offer the potential for higher oxidation efficiency and high current densities at a significantly lower cost. This makes viologen-mediated cells an appealing option for future development of glucose fuel cells. Redox Flow Battery. An asymmetric viologen called MMV was assessed for potential use in aqueous flow batteries to improve performance. With an asymmetric structure, MMV demonstrated one of the most negative redox potentials reported to date for organic electroactive compounds. MMV also showed a relatively high solubility in neutral electrolytes. The electrochemical reaction of MMV involved a reversible single electron transfer with fast kinetics. These characteristics support MMV as a promising anolyte for flow battery applications to improve capacity, energy density, and cell potential. MMV, however, exhibited poor cycling performance at elevated concentrations since it underwent irreversible or partially reversible side reactions. Signs of dimerization and precipitation were observed during cycling. These undesired reactions can be potentially mitigated by synthesizing asymmetric MMV derivatives that possess a higher charge than that possessed by MMV (+1). This modification can reduce the extent of dimerization by increasing repulsive forces between the monomers, and it also has the potential to reduce precipitation by increasing the solubility limit of the compounds.
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Iwata, Masahiro, 全広 岩田, Kimihide Hayakawa, Taro Murakami, Keiji Naruse, Keisuke Kawakami, Masumi Inoue-Miyazu, Louis Yuge, and Shigeyuki Suzuki. "Uniaxial Cyclic Stretch-Stimulated Glucose Transport Is Mediated by a Ca2+-Dependent Mechanism in Cultured Skeletal Muscle Cells." Thesis, Karger, 2007. http://hdl.handle.net/2237/11109.

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"Uniaxial Cyclic Stretch-Stimulated Glucose Transport Is Mediated by a Ca2+-Dependent Mechanism in Cultured Skeletal Muscle Cells" Pathobiology, v.74, n.3, pp.159-168を、博士論文として提出したもの。
名古屋大学博士学位論文 学位の種類:博士（リハビリテーション療法学）（課程）学位授与年月日:平成19年3月23日
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Books on the topic "Glucose-mediated"

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Klepper, Joerg. Glut1 Deficiency and the Ketogenic Diets. Edited by Eric H. Kossoff. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0005.

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Glucose is the essential fuel for the brain. Transport into brain is exclusively mediated by the facilitative glucose transporter Glut1. Glut1 deficiency results in a “brain energy crisis,” causing global developmental delay, epilepsy, and complex movement disorders including paroxysmal nonepileptic events. Early-onset absence epilepsy, paroxysmal exertion-induced dystonia, and stomatin-deficient cryohydrocytosis have been recognized as variants. Diagnosis is based on phenotype, isolated low CSF glucose, and mutations in the SLC2A1 gene. The condition is treated effectively by classical ketogenic diets providing ketones as an alternative fuel for the brain. The modified Atkins diet in adolescents and adults improves palatability and compliance at the expense of lower ketosis. Dietary treatment is continued into adolescence to meet the energy demand of the developing brain, raising concerns about long-term adverse effects. Current fields of research include novel compounds such as ketoesters and genetic approaches in Glut1-deficient mice as potential treatment options.
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Sherwood, Dennis, and Paul Dalby. The bioenergetics of living cells. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198782957.003.0024.

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Living systems create order, and appear to break the Second Law. This chapter explains, and resolves, this apparent paradox, drawing on the concept of coupled reactions (as introduced in Chapters 13 and 16), as mediated by ‘energy currencies’ such as ATP and NADH. The chapter then examines the key energy-capturing systems in biological systems – glycolysis and the citric acid cycle, and also photosynthesis. Topics covered include how energy is captured in the conversion of glucose to pyruvate, the mitochondrial membrane, respiration, electron transport, ATP synthase, chloroplasts and thylakoids, photosystems I and II, and the light-independent reactions of photosynthesis.
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Jeng, Winnie. Free radical determinants of endogenous and amphetamine-enhanced neurodegenerative disease: Prostaglandin H synthase-catalyzed free radical formation, reactive oxygen species-mediated oxidative DNA damage and glucose-6-phosphate dehydrogenase-catalyzed neuroprotection. 2004.

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O’Flaherty, Martin, Susanna Sans-Menendez, Simon Capewell, and Torben Jørgensen. Epidemiology of atherosclerotic cardiovascular disease: scope of the problem and its determinants. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0001.

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The epidemic of cardiovascular disease (CVD) in the twentieth century prompted many population-based surveys. Now, a huge number of epidemiological studies provide a clear picture of the risk for CVD. Approximately 80% of CVD can be explained by smoking, high blood pressure, and deterioration of lipid and glucose metabolism, the two latter mediated through an unhealthy diet (high intake of salt, saturated fat, and refined sugar) and physical inactivity. A causal web for CVD shows that the influence is seen throughout the life course, and that ‘upstream‘ factors like socioeconomic status, health policies, and industrial influences all have a powerful impact on the more downstream parameters like lifestyle and biomarkers. This emphasizes that population-level interventions represent the most effective options for future strategies for the prevention of CVD.
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Poff, Angela M., Shannon L. Kesl, and Dominic P. D’Agostino. Ketone Supplementation for Health and Disease. Edited by Dominic P. D’Agostino. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0032.

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Exogenous ketone supplements rapidly elevate blood ketones in a dose-dependent manner regardless of dietary intake, making them a practical method of inducing therapeutic ketosis for medical use. It is thought that ketone supplementation could be used as a stand-alone therapy, or as a way to further augment the therapeutic efficacy of the ketogenic diet. Ketone supplementation could increase treatment compliance by allowing many patients to maintain a more normal lifestyle with a less restrictive diet. The therapeutic effects of ketone supplementation are likely mediated in part by a stabilization of blood glucose and insulin levels, an increase in metabolic efficiency, and an inhibition of oxidative stress and inflammation. Ketone supplements may also serve as an effective preventative medicine due to their potential ability to protect and enhance mitochondrial health and function. Indeed, preliminary evidence suggests there are a number of conditions for which exogenous ketone supplementation may be beneficial.
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Servais, Aude. Nephropathic Cystinosis in Adults. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0060.

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Cystinosis is an autosomal recessive lysosomal storage disorder caused by a defect in the carrier-mediated system that normally transports cystine out of lysosomes. As a consequence, tissues accumulate variable amounts of the disulphide amino acid cystine. Three overlapping clinical phenotypes are recognized, varying in severity and age of onset. The most severe, the infantile nephropathic form (MIM 219800), appears in the first year of life. The late-onset form (MIM 219900) is also nephropathic, while ocular, non-nephropathic cystinosis manifests largely with corneal crystal deposition (MIM 219750). Infantile cystinosis is the most common form. Affected children develop renal proximal tubulopathy at 6 to 12 months of age. In the absence of treatment, renal failure occurs, with progression to end-stage renal disease (ESRD). Cystine crystal deposition in the cornea leads to photophobia and continuous widespread cystine accumulation eventually leads to rickets, retinal, endocrinological (hypothyroidism and impaired glucose tolerance), hepatic, gastrointestinal, muscular, and neurological abnormalities.
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Erickson, Stephen B., Hatem Amer, and Timothy S. Larson. Urolithiasis, Kidney Transplantation, and Pregnancy and Kidney Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0475.

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It was previously assumed that all kidney stones crystallized as urine passed through the renal tubules and were retained by means of crystal-tubular cell interactions. Recently uroscopy with papillary biopsies has shown 2 different pathways for stone formation, both mediated by calcium phosphate crystals. Kidney transplant has become the preferred treatment for patients with end-stage renal disease. Those benefiting from transplant included patients who would be deemed "high risk," such as those with diabetes mellitus and those older than 70 years. Anatomical changes associated with pregnancy are renal enlargement and dilatation of the calyces, renal pelvis, and ureters. Physiologic changes include a 30% to 50% increase in glomerular filtration rate and renal blood flow; a mean decrease of 0.5 mg/dL in the creatinine level and a mean decrease of 18 mg/dL in the serum urea nitrogen level; intermittent glycosuria independent of plasma glucose; proteinuria; aminoaciduria; increased uric acid excretion; increased total body water, with osmostat resetting; 50% increase in plasma volume and cardiac output; and increased ureteral peristalsis.
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Litell, John M., and Nathan I. Shapiro. Pathophysiology of septic shock. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0297.

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The pathophysiology of sepsis is the result of a dysregulated host response to infection. Interactions between conserved pathogenic signals and host recognition systems initiate a systemic reaction to local infection. Pro- and anti-inflammatory intermediates and associated coagulatory abnormalities lead to altered macrovascular, microvascular, and mitochondrial function. Uncorrected, these processes yield similar patterns of failure in multiple organ systems. Mortality increases with successive organ failures. Although commonly thought to be a manifestation of impaired renal circulation, septic acute kidney injury may be due primarily to non-haemodynamic factors. Pulmonary parenchymal dysfunction in sepsis also contributes to failures in other organ systems. Sepsis involves complex alterations in myocardial function, vascular tone, and capillary integrity, which are mediated by elevated concentrations of inflammatory cytokines, inducible nitric oxide, and reactive oxygen species, among others. Gut hypomotility and translocation of enteric flora likely contribute to a persistent inflammatory response. This perpetuates the pathophysiological pattern of sepsis, and can lead to the delayed onset of these features in patients with other types of critical illness. The neurological manifestations of sepsis include acquired delirium, which is also probably due to circulatory and inflammatory abnormalities, as well as alterations in cerebral amino acid metabolism. Critical illness-related corticosteroid insufficiency and derangements in glucose metabolism are among the endocrine abnormalities commonly seen in septic patients. Restoration of homeostasis requires early haemodynamic resuscitation and aggressive infectious source control.
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Book chapters on the topic "Glucose-mediated"

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Konrad, Daniel, Assaf Rudich, and Amira Klip. "Insulin-Mediated Regulation of Glucose Metabolism." In Insulin Resistance, 63–85. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011327.ch2.

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Shukla, Surendra K., Scott E. Mulder, and Pankaj K. Singh. "Hypoxia-Mediated In Vivo Tumor Glucose Uptake Measurement and Analysis." In Methods in Molecular Biology, 107–13. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7665-2_10.

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Martínez, F., A. Villarejo, Z. M. Ramazanov, and M. I. Orús. "Carbonic Anhydrase Independent Stimulation of Inorganic Carbon Fixation Mediated by Glucose." In Research in Photosynthesis, 803–6. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-009-0383-8_171.

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Satoh, Tadashi, and Koichi Kato. "Structural Aspects of ER Glycoprotein Quality-Control System Mediated by Glucose Tagging." In Glycobiophysics, 149–69. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-2158-0_8.

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Yelich, Michael R., Linda Witek-Janusek, and James P. Filkins. "Glucose Dyshomeostasis in Endotoxicosis Direct Versus Monokine-Mediated Mechanisms of Endotoxin Action." In Immunobiology and Immunopharmacology of Bacterial Endotoxins, 111–32. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2253-5_10.

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Chang, Min-Lee, Chung-Jung Chiu, Fu Shang, and Allen Taylor. "High Glucose Activates ChREBP-Mediated HIF-1α and VEGF Expression in Human RPE Cells Under Normoxia." In Retinal Degenerative Diseases, 609–21. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-3209-8_77.

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Lubec, G., B. Bartosch, R. Mallinger, D. Adamiker, H. Höger, and J. Gialamas. "The effect of substance L on glucose mediated cross links of collagen in the diabetic KK mouse." In Amino Acids, 670–75. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-011-2262-7_80.

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Bilan, Philip J., Toolsie Ramlal, and Amira Klip. "IGF-I Mediated Recruitment of Glucose Transporters from Intracellular Membranes to Plasma Membranes in L6 Muscle Cells." In Advances in Experimental Medicine and Biology, 273–88. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5949-4_25.

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Brown, Larry. "Glucose-Mediated Insulin Delivery from Implantable Polymers." In Polymeric Biomaterials, Revised and Expanded. CRC Press, 2001. http://dx.doi.org/10.1201/9780203904671.ch43.

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"Glucose-Mediated Insulin Delivery from Implantable Polymers." In Polymeric Biomaterials, Revised and Expanded, 1115–30. CRC Press, 2001. http://dx.doi.org/10.1201/9780203904671-45.

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Conference papers on the topic "Glucose-mediated"

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Shaikh, Saame (Raz), Anandita Pal, and Ian Carroll. "Eicosapentaenoic acid ethyl esters prevent obesity-driven impairments to glucose homeostasis through the biosynthesis of downstream hydroxylated metabolites." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/colx6433.

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There is considerable debate on the clinical utility of the long n-3 polyunsaturated fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) for preventing dysregulation of obesity-driven glucose homeostasis. Herein, we first show that administration of ethyl esters of EPA, but not DHA, to C57BL/6J male mice improves hyperglycemia, hyperinsulinemia, and glucose tolerance. Mechanistically, we demonstrate that EPA reverses the obesity-driven decrease in the concentration of white adipose tissue and liver 18-hydroxyeicosapentaenoic acid (18-HEPE), the precursor for resolvin E1 (RvE1). A combination of add-back and receptor knockout experiments reveal that RvE1 is specifically driving the improvement in hyperinsulinemia and hyperglycemia through the receptor known as ERV1/ChemR23 by controlling pathways related to hepatic glucose metabolism and inflammation. Next, we show that EPA’s effects are distinct in female mice as EPA administration leads to improvements in body weight, hyperinsulinemia and hyperglycemia but not glucose tolerance. In this case, EPA exerts its effects through a mechanism potentially mediated by 8-HEPE and upregulation of key intestinal microbes. Finally, we present translation data showing that glucose levels in humans with obesity are inversely related to EPA but not DHA in a sex-specific manner. Furthermore, data from our pilot clinical trial demonstrate that an 18-HEPE-enriched marine oil supplement increases RvE1 levels by 3-fold in humans with obesity. Taken together, these results provide clarity to the field by suggesting that EPA but not DHA ethyl esters can prevent glucose dysregulation in a sex-specific manner through distinct mechanisms mediated by downstream hydroxylated metabolites.
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Gwak, HyeRan, Jae Hong No, and Yong Sang Song. "Abstract 1851: Resveratrol impairs GLUT-1 mediated glucose uptake in ovarian cancer cells ." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1851.

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Wang, Hung-Jung, Ya-Ju Hsieh, Wen-Chi Cheng, Chun-Pu Lin, Yu-Shan Lin, So-Fang Yang, Chung-Ching Chen, et al. "Abstract 3359: JMJD5 regulates PKM2 nuclear translocation and reprograms HIF-1α-mediated glucose metabolism." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3359.

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Ara, G., D. Ohuoha, and A. R. Oseroff. "Partial Inhibition Of Glycolysis With 2-Deoxy-D-Glucose Enhances EDKC Mediated Cellular Photosensitization." In 1987 Cambridge Symposium, edited by Douglas C. Neckers. SPIE, 1988. http://dx.doi.org/10.1117/12.942712.

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Sarkodie, J., C. Asare, P. Debrah, and E. Oppong Bekoe. "Taraxacum officinale leaves aqueous extract-mediated glucose lowering effect in STZ-induced diabetic rats." In GA 2017 – Book of Abstracts. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1608450.

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Rodriguez, Olga Catalina, Vamsi Kokula, Jason Catania, Anju Preet, Arslaan Arshed,, Michael Pishvaian, Christopher Albanese, and Maria L. Avantaggiati. "Abstract 4833: Glucose restriction induces degradation of p53 mutants via a selective autophagy-mediated pathway." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4833.

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Samuel, Samson Mathews, Suparna Ghosh, Yasser Majeed, and Chris R. Triggle. "Metformin Mediated Inhibition of the mTOR Pathway Promotes Death in Glucose Starved Micro-Vascular Endothelial Cells." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2016. http://dx.doi.org/10.5339/qfarc.2016.hbpp2281.

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Tamada, Mayumi, Makoto Suematsu, and Hideyuki Saya. "Abstract 5424: CD44-mediated glucose metabolism affects ROS level and drug sensitivity in glycolytic cancer cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5424.

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Gerogianni, Irene, Rajesh Jagirdar, Eleanna Pitaraki, Olympia Kouliou, Chrissi Hatzoglou, Konstantinos Gourgoulianis, and Sotiris Zaroginannis. "Effects of 2-Deoxy-glucose (2DG) with cisplatin and pemetrexed in mesothelioma cell mediated collagen gel contraction." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.oa3800.

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Gutierrez-Avella, Dora-Marina, Michele Bertrand, and Robert Nouguier. "Stereoinduction in the Tosyl Radical-Mediated Cyclization of Polysubstituted 1,6-Dienes Derived from D-Glucose and D-Mannose." In The 4th International Electronic Conference on Synthetic Organic Chemistry. Basel, Switzerland: MDPI, 2000. http://dx.doi.org/10.3390/ecsoc-4-01792.

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Reports on the topic "Glucose-mediated"

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Granot, David, Richard Amasino, and Avner Silber. Mutual effects of hexose phosphorylation enzymes and phosphorous on plant development. United States Department of Agriculture, January 2006. http://dx.doi.org/10.32747/2006.7587223.bard.

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Research objectives 1) Analyze the combined effects of hexose phosphorylation and P level in tomato and Arabidopsis plants 2) Analyze the combined effects of hexose phosphorylation and P level in pho1 and pho2 Arabidopsis mutants 3) Clone and analyze the PHO2 gene 4) Select Arabidopsis mutants resistant to high and low P 5) Analyze the Arabidopsis mutants and clone the corresponding genes 6) Survey wild tomato species for growth characteristics at various P levels Background to the topic Hexose phosphorylating enzymes, the first enzymes of sugar metabolism, regulate key processes in plants such as photosynthesis, growth, senescence and vascular transport. We have previously discovered that hexose phosphorylating enzymes might regulate these processes as a function of phosphorous (P) concentration, and might accelerate acquisition of P, one of the most limiting nutrients in the soil. These discoveries have opened new avenues to gain fundamental knowledge about the relationship between P, sugar phosphorylation and plant development. Since both hexose phosphorylating enzymes and P levels affect plant development, their interaction is of major importance for agriculture. Due to the acceleration of senescence caused by the combined effects of hexose phosphorylation and P concentration, traits affecting P uptake may have been lost in the course of cultivation in which fertilization with relatively high P (30 mg/L) are commonly used. We therefore intended to survey wild tomato species for high P-acquisition at low P soil levels. Genetic resources with high P-acquisition will serve not only to generate a segregating population to map the trait and clone the gene, but will also provide a means to follow the trait in classical breeding programs. This approach could potentially be applicable for other crops as well. Major conclusions, solutions, achievements Our results confirm the mutual effect of hexose phosphorylating enzymes and P level on plant development. Two major aspects of this mutual effect arose. One is related to P toxicity in which HXK seems to play a major role, and the second is related to the effect of HXK on P concentration in the plant. Using tomato plants we demonstrated that high HXK activity increased leaf P concentration, and induced P toxicity when leaf P concentration increases above a certain high level. These results further support our prediction that the desired trait of high-P acquisition might have been lost in the course of cultivation and might exist in wild species. Indeed, in a survey of wild species we identified tomato species that acquired P and performed better at low P (in the irrigation water) compared to the cultivated Lycopersicon esculentum species. The connection between hexose phosphorylation and P toxicity has also been shown with the P sensitive species VerticordiaplumosaL . in which P toxicity is manifested by accelerated senescence (Silber et al., 2003). In a previous work we uncovered the phenomenon of sugar induced cell death (SICD) in yeast cells. Subsequently we showed that SICD is dependent on the rate of hexose phosphorylation as determined by Arabidopsis thaliana hexokinase. In this study we have shown that hexokinase dependent SICD has many characteristics of programmed cell death (PCD) (Granot et al., 2003). High hexokinase activity accelerates senescence (a PCD process) of tomato plants, which is further enhanced by high P. Hence, hexokinase mediated PCD might be a general phenomena. Botrytis cinerea is a non-specific, necrotrophic pathogen that attacks many plant species, including tomato. Senescing leaves are particularly susceptible to B. cinerea infection and delaying leaf senescence might reduce this susceptibility. It has been suggested that B. cinerea’s mode of action may be based on induction of precocious senescence. Using tomato plants developed in the course of the preceding BARD grant (IS 2894-97) and characterized throughout this research (Swartzberg et al., 2006), we have shown that B. cinerea indeed induces senescence and is inhibited by autoregulated production of cytokinin (Swartzberg et al., submitted). To further determine how hexokinase mediates sugar effects we have analyzed tomato plants that express Arabidopsis HXK1 (AtHXK1) grown at different P levels in the irrigation water. We found that Arabidopsis hexokinase mediates sugar signalling in tomato plants independently of hexose phosphate (Kandel-Kfir et al., submitted). To study which hexokinase is involved in sugar sensing we searched and identified two additional HXK genes in tomato plants (Kandel-Kfir et al., 2006). Tomato plants have two different hexose phosphorylating enzymes; hexokinases (HXKs) that can phosphorylate either glucose or fructose, and fructokinases (FRKs) that specifically phosphorylate fructose. To complete the search for genes encoding hexose phosphorylating enzymes we identified a forth fructokinase gene (FRK) (German et al., 2004). The intracellular localization of the four tomato HXK and four FRK enzymes has been determined using GFP fusion analysis in tobacco protoplasts (Kandel-Kfir et al., 2006; Hilla-Weissler et al., 2006). One of the HXK isozymes and one of the FRK isozymes are located within plastids. The other three HXK isozymes are associated with the mitochondria while the other three FRK isozymes are dispersed in the cytosol. We concluded that HXK and FRK are spatially separated in plant cytoplasm and accordingly might play different metabolic and perhaps signalling roles. We have started to analyze the role of the various HXK and FRK genes in plant development. So far we found that LeFRK2 is required for xylem development (German et al., 2003). Irrigation with different P levels had no effect on the phenotype of LeFRK2 antisense plants. In the course of this research we developed a rapid method for the analysis of zygosity in transgenic plants (German et al., 2003).
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