Semantic Scholar extracted view of Coupling of glutamatergic neurotransmission and neuronal glucose oxidation over the entire range of cerebral cortex activity. by Anant Bahadur Patel et al.

Brain-derived neurotrophic factor (BDNF) promotes the biochemical and morphological differentiation of selective populations of neurons during development. In this study we examined the energy requirements associated with the effects of BDNF on neuronal differentiation. Because glucose is the preferred energy substrate in the brain, the effect of BDNF on glucose utilization was investigated in developing cortical neurons via biochemical and imaging studies. Results revealed that BDNF increases glucose utilization and the expression of the neuronal glucose transporter GLUT3. Stimulation of glucose utilization by BDNF was shown to result from the activation of Na+/K+-ATPase via an increase in Na+ influx that is mediated, at least in part, by the stimulation of Na+-dependent amino acid transport. The increased Na+-dependent amino acid uptake by BDNF is followed by an enhancement of overall protein synthesis associated with the differentiation of cortical neurons. Together, these data demonstrate the

Insulin stimulates the uptake of glucose in several target tissues, including skeletal muscle and adipose tissue, thereby contributing to the decline in the blood glucose level. In this book, the authors present current research in the study of the regulation, signaling pathways and health implications of glucose uptake.. Topics include glucose uptake and transport regulation; the mechanisms that contribute to glucose homeostasis; expression and regulation of neuronal glucose transporters in health and disease; role for the microvasculature in glucose uptake in skeletal muscle; implications of diabetes on sperm glucose uptake and metabolism; the beneficial role of estrogen signaling in glucose homeostasis and energy expenditure; glucose uptake and androgen responsiveness of prostate cancer cells; regulation of intestinal glucose uptake by leptin; and the Ras superfamily of small GTP-binding proteins in glucose transporter type 4-mediated glucose uptake in insulin-responsive tissues. (Imprint: ...

In addition to the pancreatic β-cell the KATP channel resides on smooth and cardiac muscles and other nonneural tissues. The KATP channel is present on brain GR neurons but not glia (20). The Kir6.2 pore-forming unit (20, 32, 35,63) and both a high (SUR1)- and low (SUR2)-affinity form of the SUR have been cloned and identified in brain (21, 33, 49, 51, 63, 114). A presumptive endogenous ligand for the SUR, α-endosulfine, was also identified in the brain (84) but little is known about its regulation or regional distribution. Similar to the pancreatic β-cell, the KATP channel on GR neurons is inactivated by an increased intracellular ATP-to-ADP ratio or the presence of sulfonylureas. This leads to accumulation of intracellular K+ with subsequent membrane depolarization and cell firing (6, 21, 87, 89). Although it is clear that GR neurons use glucose as a signaling molecule acting via the KATP channel, several unresolved issues remain. First, the neuronal glucose transporter (GLUT-3) (26) and ...

Fibroblasts were isolated from a skin biopsy of a clinically diagnosed 51-year-old female attention-deficit/hyperactivity disorder (ADHD) patient carrying a duplication of SLC2A3, a gene encoding neuronal glucose transporter-3 (GLUT3). Patient fibroblasts were infected with Sendai virus, a single-stranded RNA virus, to generate transgene-free human induced pluripotent stem cells (iPSCs). SLC2A3-D2-iPSCs showed expression of pluripotency-associated markers, were able to differentiate into cells of the three germ layers in vitro and had a normal female karyotype. This in vitro cellular model can be used to study the role of risk genes in the pathogenesis of ADHD, in a patient-specific manner ...

Airley, Rachel, Evans, Andrew, Mobasheri, Ali and Hewitt, Stephen M. (2010) Glucose transporter Glut-1 is detectable in peri-necrotic regions in many human tumor types but not normal tissues: Study using tissue microarrays. Annals of Anatomy - Anatomischer Anzeiger, 192 (3). pp. 133-138. ISSN 0940-9602 Airley, Rachel, Loncaster, Juliette, Davidson, Susan, Bromley, Mike, Roberts, Stephen, Patterson, Adam V., Hunter, Robin, Stratford, Ian and West, Catharine M.L. (2001) Glucose transporter Glut-1 expression correlates with tumor hypoxia and predicts metastasis-free survival in advanced carcinoma of the cervix. Clinical cancer research, 7 (4). pp. 928-934. ISSN 1078-0432 Airley, Rachel, Loncaster, Juliette, Raleigh, James A., Harris, Adrian L., Davidson, Susan E., Hunter, Robert D., West, Catharine M.L. and Stratford, Ian J. (2003) GLUT-1 and CAIX as intrinsic markers of hypoxia in carcinoma of the cervix: Relationship to pimonidazole binding. International Journal of Cancer, 104 (1). pp. 85-91. ...

The facilitative glucose transporter Glut-1 is overexpressed and confers poor prognosis in a wide range of solid tumours. The peri-necrotic pattern of expression often seen in human tumour samples is linked with its transcriptional control in hypoxic conditions by hypoxia-inducible factor HIF-1 or through a reduced rate of oxidative phosphorylation. Hypoxia-regulated genes offer promise as novel therapeutic targets as a means of preventing the proliferation and eventual metastatic spread of tissue originating from residual chemically and radio resistant hypoxic cells that have survived treatment. Inhibiting the expression or functionality of Glut-1 may be a way of specifically targeting hypoxic cells within the tumour that depend upon a high rate of glucose uptake for anaerobic glycolysis. We used an array of formalin-fixed, paraffin-embedded samples of the NCI-60 panel of cell lines to carry out immunohistochemical detection of Glut-1 and to select possible candidate lead compounds by COMPARE ...

TY - JOUR. T1 - Cerebral glucose utilization and glucose transporter expression. T2 - Response to water deprivation and restoration. AU - Koehler-Stec, Ellen M.. AU - Li, Kang. AU - Maher, Fran. AU - Vannucci, Susan J.. AU - Smith, Carolyn B.. AU - Simpson, Ian A.. PY - 2000/1/1. Y1 - 2000/1/1. N2 - The relationship between local rates of cerebral glucose utilization (1CMR(glc)) and glucose transporter expression was examined during physiologic activation of the hypothalamoneurohypophysial system. Three days of water deprivation, which is known to activate the hypothalamoneurohypophysial system, resulted in increased ICMR(glc) and increased concentrations of GLUT1 and GLUT3 in the neurohypophysis; mRNA levels of GLUT1 and GLUT3 were decreased and increased, respectively. Water deprivation also increased 1CMR(glc) in the hypothalamic supraoptic and paraventricular nuclei; mRNA levels of GLUT1 and GLUT3 appeared to increase in these nuclei, but the changes did not achieve statistical significance. ...

Several studies have demonstrated that the intrinsic catalytic activity of cell surface glucose transporters is highly regulated in 3T3-L1 adipocytes expressing GLUT1 (erythrocyte/brain) and GLUT4 (adipocyte/skeletal muscle) glucose transporter isoforms. For example, inhibition of protein synthesis in these cells by anisomycin or cycloheximide leads to marked increases in hexose transport without a change in the levels of cell surface glucose transporter proteins (Clancy, B. M., Harrison, S. A., Buxton, J. M., and Czech, M. P. (1991) J. Biol. Chem. 266, 10122-10130). In the present work the exofacial hexose binding sites on GLUT1 and GLUT4 in anisomycin-treated 3T3-L1 adipocytes were labeled with the cell-impermeant photoaffinity reagent [2-3H]2-N-[4-(1-azitrifluoroethyl)benzoyl]-1,3-bis- (D-mannos-4-yloxy)-2-propylamine [( 2-3H] ATB-BMPA) to determine which isoform is activated by protein synthetic blockade. As expected, a 15-fold increase in 2-deoxyglucose uptake in response to insulin was associated

Prevalence of type 2 diabetes (T2D) is increasing worldwide. Lifestyle remains the cornerstone treatment for patients with T2D who are often overweight and sedentary.. Physical activity improves glucose metabolism of patients with T2D : increased glucose utilization during acute muscle activity and improved insulin sensitivity after regular training. The molecular mechanism underlying the effects of exercise on glucose metabolism involves the glucose transporter GLUT-4 which is regulated by physical activity.. Several studies and meta-analysis have showed that physical activity reduces HbA1c by 0.6% on average. In addition, other data suggest a decrease in cardiovascular morbidity and mortality through physical activity.. Recent recommendations for T2D management call for the practice of a structured type of endurance 150 minutes per week and muscle building 2 times per week. However, implementation of these recommendations is low, even when integrated into a therapeutic education program. ...

Insulin is secreated from beta cells of pancreatic islets. In the beta cells of pancreatic islets, insulin is synthesized and stored in granules before it is secreated. When the blood glucoes degree is increased, insulin is released instantly and severed as pro-insulin in endoplasmic Reticulum and stored as active signifier in secretory granules. When the beta cells reach the portal blood flow, the freshly released insulin goes to the liver foremost ( Jansson.,1983 ) . In liver, it inhibits hapatic glucose production ( Michael. , et al,2000 ) . Insulin is an major anabolic endocrine.. It is necessary for transmembrane conveyance of glucose and aminic acids. It indirectly supresses the blood glucose degree by diminishing glucagon which transforms animal starch to glucose in liver and skeletal musculuss which are mediated by the glucose transporter ( GLUT-4 ) . It promotes transition of glucose to triglycerides and synthesis of protein, animal starch and nucleic acid. It inhibits the activity of ...

Articular cartilage is an avascular connective tissue in which the availability of oxygen and glucose is significantly lower than synovial fluid and plasma. Glucose is an important metabolic fuel and structural precursor that plays a key role in the synthesis of extracellular matrix macromolecules in articular cartilage. However, glucose concentrations in cartilage can fluctuate depending on age, physical activity and endocrine status. Chondrocytes are glycolytic cells and must be able to sense the quantities of oxygen and glucose available to them in the extracellular matrix and respond appropriately by adjusting cellular metabolism. Consequently chondrocytes must have the capacity to survive in an extracellular matrix with limited nutrients and low oxygen tensions. The molecular mechanisms responsible for allowing chondrocytes to adapt to these harsh environmental conditions are poorly understood. In this article we present a novel dual model of oxygen and glucose sensing in chondrocytes ...

PI3-kinase signal transduction in diabetes and cancer; molecular mechanisms of cancer cell metastasis and radiation/chemotherapy resistance; tumor suppressor genes with emphasis on NHERF scaffold proteins; transgenic mouse models Current studies in our lab focus on: -Identification of molecular signals targeting the activity and surface expression of insulin-sensitive glucose transport proteins (phosphorylation, ubiquitination, endosomal recycling) -Functional characterization and localization of facilitative glucose transporter GLUT12 in tumor cells -Role of nutrient (glucose) uptake in decreased sensitivity to radiation and chemotherapy: contribution of glucose transporters to radiation survival, glucose transporter expression levels as a predictive marker of radioresistance -Significance of NHERF/Akt/SGK interaction in cancer cell growth and metastasis -Generation of transgenic mouse ...

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ISHIKAWA Nobuhisa , OGURI Tetsuya , ISOBE Takeshi , FUJITAKA Kazunori , KOHNO Nobuoki Japanese journal of cancer research : gann 92(8), 874-879, 2001-08-31 医中誌Web 参考文献32件 ...

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Herein, employing anatomical and dynamic contrast-enhanced (DCE) magnetic resonance imaging (MRI), we evaluated non-invasively, the in vivo, chemopreventive efficacy of inositol hexaphosphate (IP6), a major constituent of high fiber diets, against prostate tumor growth and progression in transgenic adenocarcinoma of the mouse prostate (TRAMP) model. Male TRAMP mice, beginning 4 weeks of age, were fed with 1, 2 or 4% (w/v) IP6 in drinking water or only drinking water till 28 weeks of age and monitored using MRI over the course of study. Longitudinal assessment of prostate volumes by conventional MRI and tumor vascularity by gadolinium-based DCE-MRI showed a profound reduction in tumor size partly due to anti-angiogenic effects by IP6 treatment. As potential mechanisms of IP6 efficacy, decrease in the expression of glucose transporter GLUT-4 protein together with an increase in levels of phospho-AMP-activated kinase (AMPKTh172) were observed in prostate tissues of mice from IP6 fed-groups, ...

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ウサギ・ポリクローナル抗体 ab41525 交差種: Ms,Rat,Hu 適用: WB,IP,ELISA,IHC-P,IHC-Fr,Dot,IHC-FrFl…Glucose Transporter…

We demonstrated the specificity of the GLUT4 antagonist, indinavir, in cultured cells and observed that inhibition of GLUT4 in endothelium-denuded mouse aortas reduced basal glucose uptake by approximately half, supporting the conclusion that GLUT4 is a major glucose transporter that participates in basal, as well as in insulin-stimulated, glucose uptake in VSMCs in vivo. We also found that GLUT4 and other glucose transporters specifically and differentially contribute to VSMC contraction. Moreover, this differential contribution to contraction varies depending on the contractile agonist. We also observed that GLUT4 expression in vessels from hypertensive animals was diminished, and that indinavir caused a less profound attenuation of maximal 5-HT-mediated contraction in these vessels. We have found that chronic knockout of the GLUT4 gene results in augmented arterial reactivity to the same agonists that elicited attenuated reactivity in response to indinavir. Similar increases in reactivity ...

Glucose transport across the chondrocyte membrane is essential for chondrogenesis and the development of the skeletal system. We have previously used RT-PCR to show that fully developed human articular chondrocytes express transcripts for the GLUT1 and GLUT9 glucose transporters. In this study we report on the expression and immunohistochemical localization of the GLUT1 and GLUT9 proteins in embryonic and mature ovine cartilage. We also provide Western blot evidence for GLUT1 and GLUT9 expression in mature ovine chondrocytes. Ovine embryos (developmental stages E32 to E36 and E42 to E45) were obtained from pregnant ewes humanely killed by injection with sodium pentobarbitone. Embryos were fixed and processed for immunohistochemistry. Polyclonal antibodies to GLUT1 and GLUT9 revealed that both transporters are expressed in developing chondrocytes in ovine embryos and in the superficial, middle and deep layers of ovine cartilage from mature animals. GLUT1 expression was observed in erythrocytes ...

We have shown that Vitamin C therapy has different consequences in healthy MK-8245 distributorand collagen VI deficient fibroblasts and this could underlie some

Complementary DNA encoding a facilitative glucose transporter was isolated from a human hepatoma cell line (HepG2) cDNA library and subcloned into a metal-inducible mammalian expression vector, pLEN (California Biotechnology) containing human metallothionein gene II promoter sequences. Chinese hamster ovary (CHO) cells transfected with this transporter expression vector, pLENGT, exhibited a 2-17-fold increase in immunoreactive HepG2-type glucose transporter protein, as measured by protein immunoblotting with antipeptide antibodies directed against the HepG2-type glucose transporter C-terminal domain. Expression of the human glucose transporter was verified by protein immunoblotting with a mouse polyclonal antiserum that recognizes the human but not the rodent HepG2-type transporter. 2-Deoxy-D-glucose uptake was increased 2-7-fold in transfected cell lines. Polyclonal antisera directed against purified red blood cell glucose transporter were raised in several rabbits. Antiserum from one rabbit, delta,

The subject invention concerns materials and methods for treating oncological disorders in a person or animal using any agent or compound that inhibits uptake of glucose into a cell. The subject invention also concerns methods for inducing apoptosis and inhibiting the proliferation or survival of a cell. In one embodiment, the methods comprise administering an effective amount of an agent or compound that inhibits the activity of one or more glucose transporter proteins, such as Glut-1. An antibody that binds to and inhibits a glucose transporter protein can be used in the present methods.

Fanconi-Bickel syndrome (FBS, OMIM 227810) is a rare autosomal recessive disease caused by a deficiency of glucose transporter 2 (GLUT2), a member of the facilitative glucose transporter family (Santer et al. J Inherit Metab Dis 21:191-194, 1998). The typical clinical picture is characterized .... ...

Glucose transporter type 1 (GLUT1) antibody | P11166 | Solute carrier family 2, facilitated glucose transporter member 1, Glucose transporter type 1, erythrocyte/brain (GLUT-1), HepG2 glucose transporter, GLUT1

250 µCi quantities of 2-[14C(U)]-Deoxy-D-Glucose (300-350mCi/mmol) are available for your research. Application of [14C]Deoxy-D-Glucose can be found in: glucose transporter isoform GLUT4 gene regulation and mechanisms in insulin resistance, selectively suppressing the quinolinic acid-induced enhancement of anaerobic glycolysis in glial cells, stimulatory effect of d-ephedrine on ß3-adrenoceptors in adipose tissue of rats, glucose utilization in the brain during acute seizure as a useful biomarker for the evaluation of anticonvulsants, etc. ...

250 µCi quantities of 2-[14C(U)]-Deoxy-D-Glucose (300-350mCi/mmol) are available for your research. Application of [14C]Deoxy-D-Glucose can be found in: glucose transporter isoform GLUT4 gene regulation and mechanisms in insulin resistance, selectively suppressing the quinolinic acid-induced enhancement of anaerobic glycolysis in glial cells, stimulatory effect of d-ephedrine on ß3-adrenoceptors in adipose tissue of rats, glucose utilization in the brain during acute seizure as a useful biomarker for the evaluation of anticonvulsants, etc. ...

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Type 2 diabetes is one of the most common diseases in America and carries an enormous impact on public health, having reached epidemic proportions worldwide. Ty...

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The facilitative glucose transport protein GLUT1 has important roles in positron emission tomography (PET) imaging of human diseases

In this study, echocardiography was used to monitor the progression of LV hypertrophy and to determine the timing for the study of glucose uptake and glucose transporter protein content. The observations derived from this investigation reveal that a decrease in glucose uptake rate is evident early in the transition from compensated to decompensated pressure-overload hypertrophy, as determined by an index of LV M/V ratio. The defect in insulin-stimulated glucose uptake precedes the downregulation of sarcoplasmic reticulum Ca-ATPase (SERCA-2) and glucose transporter expression (GLUT-4 and GLUT-1).15 26 Under pathophysiological conditions such as hypertrophy or during ischemia and early reperfusion, a high rate of cardiac glucose metabolism may be crucial.27 28 29 Glucose transport is thought to be rate-limiting for glucose use. In the heart, 2 distinctive glucose transporters are responsible for glucose uptake across the plasma membrane. The GLUT-1 transporter, which is present in low levels in ...

The regulation of blood glucose levels in humans, in response to insulin, is essential to survival. This response is mediated through the insulin responsive glucose transporter GLUT4. In response to insulin stimulation GLUT4 is trafficked from intracellular insulin sensitive stores (GSVs GLUT4 storage vesicles) to the plasma membrane of fat and muscle cells allowing uptake of glucose into these cells and lowering of plasma glucose levels. Previous work from our lab has identified that ubiquitination and subsequent deubiquitination of GLUT4 is required for entry and stability in GSVs. This balance of ubiquitination and deubiquitination in mammalian cells is carried out by E3 ligases and deubiqutinating enzymes (DUBs). It appears that E3 ligases allow for targeted entry of GLUT4 into insulin sensitive GSVs and that the DUB USP25 is required for GLUT4 to stably maintained in these GSVs. Using a model developed in our lab my thesis looked at key steps of ubiquitination and deubiquitination to try ...

The effect of insulinopenic diabetes on the expression of glucose transporters in the small intestine was investigated. Enterocytes were sequentially isolated from jejunum and ileum of normal fed rats, streptozotocin-diabetic rats, and diabetic rats treated with insulin. Facilitative glucose transporter (GLUT) 2, GLUT5, and sodium-dependent glucose transporter 1 protein content was increased from 1.5- to 6-fold in enterocytes isolated from diabetic animals in both jejunum and ileum. Insulin was able to reverse the increase in transporter protein expression seen after induction of diabetes. There was a four- to eightfold increase in the amount of enterocyte glucose transporter mRNA after diabetes with greater changes in sodium-dependent glucose transporter 1 and GLUT2 than in GLUT5 levels. In situ hybridization showed that after the induction of diabetes there was new hybridization in lower villus and crypt enterocytes that was reversed by insulin treatment. Thus, the increase in total hexose ...

Abstract. Diabetes mellitus (DM) is a metabolic diseases characterized by hyperglycemia due to insufficient or inefficient insulin secretory response. This chronic disease is a global problem and there is a need for greater emphasis on therapeutic strategies in the health system. Phytochemicals such as flavonoids have recently attracted attention as source materials for the development of new antidiabetic drugs or alternative therapy for the management of diabetes and its related complications. The antidiabetic potential of flavonoids are mainly through their modulatory effects on glucose transporter by enhancing GLUT-2 expression in pancreatic β cells and increasing expression and promoting translocation of GLUT-4 via PI3K/AKT, CAP/Cb1/TC10 and AMPK pathways. This review highlights the recent findings on beneficial effects of flavonoids in the management of diabetes with particular emphasis on the investigations that explore the role of these compounds in modulating glucose transporter ...

TY - JOUR. T1 - DHHC7 palmitoylates glucose transporter 4 (Glut4) and regulates Glut4 membrane translocation. AU - Du, Keyong. AU - Murakami, Shoko. AU - Sun, Yingmin. AU - Kilpatrick, Casey L.. AU - Luscher, Bernhard. PY - 2017/2/17. Y1 - 2017/2/17. N2 - Insulin-dependent translocation of glucose transporter 4 (Glut4) to the plasma membrane plays a key role in the dynamic regulation of glucose homeostasis.Werecently showed that this process is critically dependent on palmitoylation of Glut4 at Cys-223. To gain further insights into the regulation of Glut4 palmitoylation, we set out to identify the palmitoyl acyltransferase (PAT) involved. Here we report that among 23 mammalian DHHC proteins, DHHC7 is the major Glut4 PAT, based on evidence that ectopic expression of DHHC7 increased Glut4 palmitoylation, whereas DHHC7 knockdown in 3T3-L1 adipocytes andDHHC7KOin adipose tissue and muscle decreased Glut4 palmitoylation. Moreover, inactivation of DHHC7 suppressed insulin-dependent Glut4 membrane ...

Vitamin C concentrations in the brain exceed those in blood by 10-fold. In both tissues, the vitamin is present primarily in the reduced form, ascorbic acid. We identified the chemical form of vitamin C that readily crosses the blood-brain barrier, and the mechanism of this process. Ascorbic acid was not able to cross the blood-brain barrier in our studies. In contrast, the oxidized form of vitamin C, dehydroascorbic acid (oxidized ascorbic acid), readily entered the brain and was retained in the brain tissue in the form of ascorbic acid. Transport of dehydroascorbic acid into the brain was inhibited by d-glucose, but not by l-glucose. The facilitative glucose transporter, GLUT1, is expressed on endothelial cells at the blood-brain barrier, and is responsible for glucose entry into the brain. This study provides evidence showing that GLUT1 also transports dehydroascorbic acid into the brain. The findings define the transport of dehydroascorbic acid by GLUT1 as a mechanism by which the brain ...

The oxidation of glucose represents a major source of metabolic energy for mammaliancells. However, because the plasma membrane is impermeable to polar molecules such as glucose, the cellular uptake of this important nutrient is accomplished by membrane-associated carrier proteins that bind and transfer it across the lipid bilayer. Two classes of glucose carriers have been described in mammalian cells: the Na+-glucose cotransporter and the facilitative glucose transporter. The Na+-glucose cotransporter transports glucose against its concentration gradient by coupling its uptake with the uptake of Na+ that is being transported down its concentration gradient. Facilitative glucose c rriers accelerate the transport of glucose down its concentration gradient by facilitative diffusion, a form of passive transport. cDNAs have been isolated from human tissues encoding a Na+-glucose-cotransporter protein and five functional facilitative glucosetransporter isoforms. The Na+-glucose cotransporter is ...

Glucose Transporter Inhibitor IV, WZB117 - CAS 1223397-11-2 - Calbiochem Glucose Transporter Inhibitor IV, WZB117, CAS 1223397-11-2, is a fast-acting, irreversible blocker of GLUT1 in RBCs. Also inhibits glucose transport in cancer cells (IC50 ~ 500 nM in A549 cells). - Find MSDS or SDS, a COA, data sheets and more information.

Facilitative glucose transporter. This isoform likely mediates the bidirectional transfer of glucose across the plasma membrane of hepatocytes and is responsible for uptake of glucose by the beta cells; may comprise part of the glucose-sensing mechanism of the beta cell. May also participate with the Na(+)/glucose cotransporter in the transcellular transport of glucose in the small intestine and kidney ...

Background Elevated glucose transporter 1 (GLUT1) expression and glucose utilization that come with pressure overload\induced hypertrophy (POH) are thought to be cardioprotective. mRNA appearance of oxidative phosphorylation (OXPHOS) genes had been low in Cont mice, but had been maintained in collaboration with elevated glucose usage in G1HA pursuing TAC. Despite attenuated undesirable redecorating in G1HA in accordance with control TAC mice, cardiac hypertrophy was exacerbated in these mice, and positive dP/dt (in vivo) and cardiac power (ex girlfriend or boyfriend vivo) had been equivalently reduced in Cont and G1HA TAC mice in comparison to shams, in keeping with still left ventricular dysfunction. O\GlcNAcylation of Ca2+ bicycling proteins was elevated in G1HA TAC hearts. Conclusions Brief\term cardiac particular induction of GLUT1 on the starting point of POH preserves mitochondrial function and attenuates pathological redecorating, but exacerbates the hypertrophic phenotype and it is ...

Similar to what has been shown for the Na+-coupled glucose transporter 1 (SGLT1) (31), SGK1 stimulates the facilitated glucose transporter GLUT1 by enhancing transporter abundance in the plasma membrane. The effect requires the catalytical activity of the kinase. SGK1 shuttles between cytoplasm and nucleus in a stimulus-dependent manner (38). The serum-induced nuclear import of SGK1 suggests that SGK1 acts at a transcriptional level. In fact, SGK1 has been shown to modulate the forkhead transcription factor FKHRL1 (39). Thus, SGK1 might regulate glucose transport in part by increasing GLUT1 transcript levels. However, the stimulation of glucose transport in Xenopus oocytes point to posttranscriptional regulation of GLUT1, as GLUT1 mRNA has been injected thus circumventing transcription. In addition, Western blotting of whole-cell lysates exclude GLUT1 regulation at a translational level.. SGK1 is not effective through phosphorylation of GLUT1, since the Ser-to-Ala mutation in the SGK consensus ...

Abnormalities of the glucose transporter at the blood-brain barrier and in brain in Alzheimers disease.: We have previously demonstrated the glucose transporte

Insulin and GLUT 4 - A signal transduction pathway. What is GLUT 4. Glucose transporter type 4, also known as GLUT4, is a protein that in humans is encoded by the GLUT4 gene. GLUT4 is the...

I have heard that there is a distributor for antibodies directed against the Glut-1 glucose-transporter (erythroid/brain or perivenular hepatocytes). Does anyone know this distributor ? Thanks in advance ##################################################################### # # # Dr. F.Gaunitz __________ # # Physiologisch-Chemisches Institut I I # # Universitaet Tuebingen I \/ I # # Hoppe-Seyler-Str. 4 I U /\ T I # # 72076 Tuebingen I / \ I # # Germany \ + + / # # \______/ # # e-mail: cbkga01 at mailserv.zdv.uni-tuebingen.de ...