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Glucose transporter deficiency

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https://www.readbyqxmd.com/read/28202352/amino-acid-transporter-slc38a3-promotes-metastasis-of-non-small-cell-lung-cancer-cells-by-activating-pdk1
#1
Yanhui Wang, Li Fu, Minqing Cui, Yongbin Wang, Yan Xu, Molin Li, Jun Mi
BACKGROUND: Tumor metastasis is a finely-tuned pathological process coupled to metabolic reprogramming that includes both glutamine and glucose. The solute carrier SLC38A3, a member of amino acid/polyamine/organocation (APC) superfamily, is an L-glutamine transporter. It is not clear whether SLC38A3 involves the metastasis of NSCLC (non small cell lung cancer). METHODS: The scratch test and transwell assay were used to determine the ability of NSCLC to migrate. Cellular amino acids content was determined by mass spectrometry...
February 12, 2017: Cancer Letters
https://www.readbyqxmd.com/read/28192604/dapagliflozin-lowered-blood-glucose-reduces-respiratory-p-aeruginosa-infection-in-diabetic-mice
#2
Annika Åstrand, Cecilia Wingren, Audra Benjamin, John S Tregoning, James P Garnett, Helen Groves, Simren Gill, Maria Orogo-Wenn, Anders J Lundqvist, Dafydd Walters, David M Smith, John D Taylor, Emma H Baker, Deborah L Baines
BACKGROUND AND PURPOSE: Hyperglycaemia increases glucose concentrations in airway surface liquid (ASL) and increases the risk of pulmonary Pseudomonas aeruginosa infection. We determined whether reduction of blood and airway glucose concentrations by the anti-diabetic drug dapagliflozin could reduce P. aeruginosa growth/survival in the lungs of diabetic mice. EXPERIMENTAL APPROACH: The effect of dapagliflozin on blood and airway glucose concentration, the inflammatory response and infection were investigated in C57BL/6 J (wild type, WT) or db/db (leptin receptor-deficient) mice, treated orally with dapagliflozin prior to intranasal dosing with lipopolysaccharide (LPS) or inoculation with P...
February 13, 2017: British Journal of Pharmacology
https://www.readbyqxmd.com/read/28178390/metabolic-and-hemodynamic-effects-of-sodium-dependent-glucose-co-transporter-2-inhibitors-on-cardio-renal-protection-in-the-treatment-of-patients-with-type-2-diabetes-mellitus
#3
REVIEW
Atsunori Kashiwagi, Hiroshi Maegawa
The specific Na+/glucose co-transporter 2 inhibitors (SGLT2 inhibitors) inhibit glucose reabsorption in proximal renal tubular cells, and both fasting and postprandial glucose significantly decrease due to urinary glucose loss. As a result, pancreatic β-cell function and peripheral insulin action significantly improve with relief from glucose toxicity. Furthermore, whole body energy metabolism changes to relative glucose deficiency and triggers increased lipolysis in fat cells, and fatty acid oxidation and then ketone body production in the liver during treatment with SGLT2 inhibitors...
February 8, 2017: Journal of Diabetes Investigation
https://www.readbyqxmd.com/read/28129950/eeg-findings-during-paroxysmal-hemiplegia-in-a-patient-with-glut1-deficiency
#4
S Pellegrin, G Cantalupo, R Opri, B Dalla Bernardina, F Darra
BACKGROUND: A growing number of studies have disclosed the myriad of features that can suggest the diagnosis of a Glucose-transporter-1 deficiency (GLUT1D). The occurrence of paroxysmal movement disorders such as exercise-induced dystonia and non-kinesigenic dyskinesia, received considerable emphasis, while limited attention has been paid to other paroxysmal phenomena, as transitory neurological disorders. These paroxysmal events are roughly and variably described as limb weakness, hemiparesis or ataxia...
January 17, 2017: European Journal of Paediatric Neurology: EJPN
https://www.readbyqxmd.com/read/28128227/sodium-myoinositol-cotransporter-1-smit1-mediates-the-production-of-reactive-oxygen-species-induced-by-hyperglycemia-in-the-heart
#5
Anne Van Steenbergen, Magali Balteau, Audrey Ginion, Laura Ferté, Sylvain Battault, Christophe de Meester de Ravenstein, Jean-Luc Balligand, Evangelos-Panagiotis Daskalopoulos, Patrick Gilon, Florin Despa, Sanda Despa, Jean-Louis Vanoverschelde, Sandrine Horman, Hermann Koepsell, Gerard Berry, Louis Hue, Luc Bertrand, Christophe Beauloye
Hyperglycemia (HG) stimulates the production of reactive oxygen species in the heart through activation of NADPH oxidase 2 (NOX2). This production is independent of glucose metabolism but requires sodium/glucose cotransporters (SGLT). Seven SGLT isoforms (SGLT1 to 6 and sodium-myoinositol cotransporter-1, SMIT1) are known, although their expression and function in the heart remain elusive. We investigated these 7 isoforms and found that only SGLT1 and SMIT1 were expressed in mouse, rat and human hearts. In cardiomyocytes, galactose (transported through SGLT1) did not activate NOX2...
January 27, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28126686/partial-correction-of-neutrophil-dysfunction-by-oral-galactose-therapy-in-glycogen-storage-disease-type-ib
#6
Rudolf Letkemann, Helmut Wittkowski, Aristotelis Antonopoulos, Teodor Podskabi, Stuart M Haslam, Dirk Föll, Anne Dell, Thorsten Marquardt
Glycogen storage disease type Ib (GSD-Ib) is characterized by impaired glucose homeostasis, neutropenia and neutrophil dysfunction. Mass spectrometric glycomic profiling of GSD-Ib neutrophils showed severely truncated N-glycans, lacking galactose. Experiments indicated the hypoglycosylation of the electron transporting subunit of NADPH oxidase, which is crucial for the defense against bacterial infections. In phosphoglucomutase 1 (PGM1) deficiency, an inherited disorder with an enzymatic defect just one metabolic step ahead, hypogalactosylation can be successfully treated by dietary galactose...
January 23, 2017: International Immunopharmacology
https://www.readbyqxmd.com/read/28119822/gene-therapy-for-a-mouse-model-of-glucose-transporter-1-deficiency-syndrome
#7
Sachie Nakamura, Hitoshi Osaka, Shin-Ichi Muramatsu, Naomi Takino, Mika Ito, Shiho Aoki, Eriko F Jimbo, Kuniko Shimazaki, Tatsushi Onaka, Sumio Ohtsuki, Tetsuya Terasaki, Takanori Yamagata
OBJECTIVE: We generated an adeno-associated virus (AAV) vector in which the human SLC2A1 gene was expressed under the synapsin I promoter (AAV-hSLC2A1) and examined if AAV-hSLC2A1 administration can lead to functional improvement in GLUT1-deficient mice. METHODS: AAV-hSLC2A1 was injected into heterozygous knock-out murine Glut1 (GLUT1(+/-)) mice intraperitoneally (systemic; 1.85 × 10(11) vg/mouse) or intra-cerebroventricularly (local; 1.85 × 10(10) vg/mouse)...
March 2017: Molecular Genetics and Metabolism Reports
https://www.readbyqxmd.com/read/28117144/review-alterations-in-placental-glycogen-deposition-in-complicated-pregnancies-current-preclinical-and-clinical-evidence
#8
REVIEW
Lisa K Akison, Marloes Dekker Nitert, Vicki L Clifton, Karen M Moritz, David G Simmons
Normal placental function is essential for optimal fetal growth. Transport of glucose from mother to fetus is critical for fetal nutrient demands and can be stored in the placenta as glycogen. However, the function of this glycogen deposition remains a matter of debate: It could be a source of fuel for the placenta itself or a storage reservoir for later use by the fetus in times of need. While the significance of placental glycogen remains elusive, mounting evidence indicates that altered glycogen metabolism and/or deposition accompanies many pregnancy complications that adversely affect fetal development...
January 11, 2017: Placenta
https://www.readbyqxmd.com/read/28106060/brain-microvasculature-defects-and-glut1-deficiency-syndrome-averted-by-early-repletion-of-the-glucose-transporter-1-protein
#9
Maoxue Tang, Guangping Gao, Carlos B Rueda, Hang Yu, David N Thibodeaux, Tomoyuki Awano, Kristin M Engelstad, Maria-Jose Sanchez-Quintero, Hong Yang, Fanghua Li, Huapeng Li, Qin Su, Kara E Shetler, Lynne Jones, Ryan Seo, Jonathan McConathy, Elizabeth M Hillman, Jeffrey L Noebels, Darryl C De Vivo, Umrao R Monani
Haploinsufficiency of the SLC2A1 gene and paucity of its translated product, the glucose transporter-1 (Glut1) protein, disrupt brain function and cause the neurodevelopmental disorder, Glut1 deficiency syndrome (Glut1 DS). There is little to suggest how reduced Glut1 causes cognitive dysfunction and no optimal treatment for Glut1 DS. We used model mice to demonstrate that low Glut1 protein arrests cerebral angiogenesis, resulting in a profound diminution of the brain microvasculature without compromising the blood-brain barrier...
January 20, 2017: Nature Communications
https://www.readbyqxmd.com/read/28090774/biakamides-a-d-unique-polyketides-from-a-marine-sponge-act-as-selective-growth-inhibitors-of-tumor-cells-adapted-to-nutrient-starvation
#10
Naoyuki Kotoku, Ryosuke Ishida, Hirokazu Matsumoto, Masayoshi Arai, Kazunari Toda, Andi Setiawan, Osamu Muraoka, Motomasa Kobayashi
Biakamides A-D, novel unusually unique polyketides, were isolated from an Indonesian marine sponge (Petrosaspongia sp.) with a constructed bioassay using PANC-1 human pancreatic cancer cells. Through detailed analyses of the one- and two-dimensional NMR spectra of biakamides, planar chemical structures possessing a terminal thiazole, two N-methyl amides, a chloromethylene, and a substituted butyryl moiety were obtained. After elucidation of the configuration of the secondary alcohol moiety in biakamides A and B, the absolute stereostructures of the two secondary methyl groups in biakamides A-D were determined by the asymmetric total syntheses of all possible stereoisomers from the optically pure monoprotected 2,4-dimethyl-1,5-diol...
January 25, 2017: Journal of Organic Chemistry
https://www.readbyqxmd.com/read/28070879/a-review-of-pharmacogenetics-of-antimalarials-and-associated-clinical-implications
#11
REVIEW
Hazem Elewa, Kyle John Wilby
Genetic variability in drug-metabolizing enzymes and drug transporters is known to influence the pharmacokinetics of many drugs. Antimalarial drugs are a class of agents known to utilize metabolic and elimination pathways prone to genetic variation. This paper aims to review the genetic variants affecting antimalarial medications and discuss their clinical implications. Data were identified for the genes coding for the cytochrome P450 (CYP) enzymes: CYP2C8, CYP2C19, CYP2A6, CYP2D6, CYP2B6, and the P-glycoprotein drug transporter...
January 9, 2017: European Journal of Drug Metabolism and Pharmacokinetics
https://www.readbyqxmd.com/read/28070695/barth-syndrome-connecting-cardiolipin-to-cardiomyopathy
#12
REVIEW
Nikita Ikon, Robert O Ryan
The Barth syndrome (BTHS) is caused by an inborn error of metabolism that manifests characteristic phenotypic features including altered mitochondrial membrane phospholipids, lactic acidosis, organic acid-uria, skeletal muscle weakness and cardiomyopathy. The underlying cause of BTHS has been definitively traced to mutations in the tafazzin (TAZ) gene locus on chromosome X. TAZ encodes a phospholipid transacylase that promotes cardiolipin acyl chain remodeling. Absence of tafazzin activity results in cardiolipin molecular species heterogeneity, increased levels of monolysocardiolipin and lower cardiolipin abundance...
February 2017: Lipids
https://www.readbyqxmd.com/read/28068143/adaptations-to-excess-choline-in-insulin-resistant-and-pcyt2-deficient-skeletal-muscle
#13
Adrian Taylor, Laila Cigana Schenkel, Maiya Yokich, Marica Bakovic
It was hypothesized that choline supplementation in insulin resistant (IR) CTP:phosphoethanolamine cytidylyltransferase deficient (Pcyt2(+/-)) mice would ameliorate muscle function by remodeling glucose and fatty acid (FA) metabolism. Pcyt2(+/-) mice either received no treatment or were allowed access to 2 mg/mL choline in drinking water for 4 weeks. Skeletal muscle was harvested from choline treated and untreated mice. Lipid analysis and metabolic gene expression and signaling pathways were compared between untreated Pcyt2(+/-) mice, treated Pcyt2(+/-) mice, and Pcyt2(+/+) mice...
September 6, 2016: Biochemistry and Cell Biology, Biochimie et Biologie Cellulaire
https://www.readbyqxmd.com/read/28056409/efficacy-of-metformin-in-human-single-hair-fibre-by-atr-ftir-spectroscopy-coupled-with-statistical-analysis
#14
Kamatchi Sundaramoorthi, Gunasekaran Sethu, Sailatha Ethirajulu, Pavithra Raja Marthandam
Diabetes mellitus is chronic metabolic disorder, resulting from insulin deficiency, characterized by hyperglycemia altered metabolism of carbohydrates, proteins and lipids and an increased risk of vascular complications. There are different classes of anti-diabetic drugs in allopathic system of medicine. Metformin (dimethyl biguanide) is a blood glucose lowering agent used in the treatment of non-insulin dependent diabetes mellitus. Almost in all diseases the blood serves as the primary metabolic transport system in the body...
March 20, 2017: Journal of Pharmaceutical and Biomedical Analysis
https://www.readbyqxmd.com/read/28040509/integration-of-proteomics-and-metabolomics-to-elucidate-metabolic-adaptation-in-leishmania
#15
Snezhana Akpunarlieva, Stefan Weidt, Dhilia Lamasudin, Christina Naula, David Henderson, Michael Barrett, Karl Burgess, Richard Burchmore
: Leishmania parasites multiply and develop in the gut of a sand fly vector in order to be transmitted to a vertebrate host. During this process they encounter and exploit various nutrients, including sugars, and amino and fatty acids. We have previously generated a mutant Leishmania line that is deficient in glucose transport and which displays some biologically important phenotypic changes such as reduced growth in axenic culture, reduced biosynthesis of hexose-containing virulence factors, increased sensitivity to oxidative stress, and dramatically reduced parasite burden in both insect vector and macrophage host cells...
December 29, 2016: Journal of Proteomics
https://www.readbyqxmd.com/read/28018440/glucose-transport-1-deficiency-presenting-as-infantile-spasms-with-a-mutation-identified-in-exon-9-of-slc2a1
#16
Hyun Hee Lee, Yun Jung Hur
Glucose transport 1 (GLUT-1) deficiency is a rare syndrome caused by mutations in the glucose transporter 1 gene (SLC2A1) and is characterized by early-onset intractable epilepsy, delayed development, and movement disorder. De novo mutations and several hot spots in N34, G91, R126, R153, and R333 of exons 2, 3, 4, and 8 of SLC2A1 are associated with this condition. Seizures, one of the main clinical features of GLUT-1 deficiency, usually develop during infancy. Most patients experience brief and subtle myoclonic jerk and focal seizures that evolve into a mixture of different types of seizures, such as generalized tonic-clonic, absence, myoclonic, and complex partial seizures...
November 2016: Korean Journal of Pediatrics
https://www.readbyqxmd.com/read/28008588/losartan-improves-palmitate-induced-insulin-resistance-in-3t3-l1-adipocytes-through-upregulation-of-src-phosphorylation
#17
X Tian, M Ye, Y Cao, C Wang
Angiotensin II type 1 receptor blocker losartan has shown strongly anti-insulin resistance properties in vivo and in vitro; however, the underlying mechanisms are poorly understood. In this study, we demonstrate that losartan administration increased phosphorylation of Akt and its downstream Akt substrate of 160 kDa (AS160), enhanced plasma membrane translocation of glucose transporter type 4 (GLUT4), and increased glucose uptake, along with increased Src phosphorylation as well as reduced expression of docking protein 1(DOK1) in palmitate-treated 3T3-L1 adipocytes...
December 22, 2016: Experimental and Clinical Endocrinology & Diabetes
https://www.readbyqxmd.com/read/28000448/glycoconjugated-site-selective-dna-methylating-agent-targeting-glucose-transporters-on-glioma-cells
#18
Mairin K Buchanan, Chase N Needham, Nina E Neill, Maria C White, Charles B Kelly, Kelly Mastro-Kishton, Lacie M Chauvigne-Hines, Tyler J Goodwin, Andrew L McIver, Libero J Bartolotti, Arthur R Frampton, Andrea J Bourdelais, Sridhar Varadarajan
DNA-alkylating drugs continue to remain an important weapon in the arsenal against cancers. However, they typically suffer from several shortcomings because of the indiscriminate DNA damage that they cause and their inability to specifically target cancer cells. We have developed a strategy for overcoming the deficiencies in current DNA-alkylating chemotherapy drugs by designing a site-specific DNA-methylating agent that can target cancer cells because of its selective uptake via glucose transporters, which are overexpressed in most cancers...
January 3, 2017: Biochemistry
https://www.readbyqxmd.com/read/27984051/brain-endothelial-dysfunction-following-pyrithiamine-induced-thiamine-deficiency-in-the-rat
#19
Sumit Sarkar, Serguei Liachenko, Merle G Paule, John Bowyer, Joseph P Hanig
Prolonged vitamin B1 (thiamine) deficiency can lead to neurological disorders such as Wernicke's encephalopathy and Wernicke-Korsakoff Syndrome (WKS) in humans. These thiamine deficiency disorders have been attributed to vascular leakage, blood-brain barrier breakdown and neuronal loss in the diencephalon and brain stem. However, endothelial dysfunction following thiamine deficiency and its relationship to the phenomenon of neurodegeneration has not been clearly elucidated. The present study sought to begin to address this issue by evaluating vascular morphology and integrity in a pyrithiamine (PT)-induced rat model of thiamine deficiency...
October 28, 2016: Neurotoxicology
https://www.readbyqxmd.com/read/27975114/the-ketogenic-diet-a-practical-guide-for-pediatricians
#20
Aimee F Luat, Leigh Coyle, Deepak Kamat
The ketogenic diet is an effective treatment for drug-resistant epilepsies in children. In addition, it is the first-line treatment for some metabolic disorders, such as glucose transporter 1 deficiency syndrome. This article discusses the proposed mechanisms of a ketogenic diet's antiseizure action, its clinical indications, and its contraindications. The steps involved in ketogenic diet initiation, monitoring, and management of its side effects are also discussed. This review provides general pediatricians with the necessary skills to provide comprehensive care of children using the ketogenic diet and counsel their families and caregivers...
December 1, 2016: Pediatric Annals
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