scholarly journals The low affinity glucose transporter HxtB is also involved in glucose signalling and metabolism in Aspergillus nidulans

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Thaila Fernanda dos Reis ◽  
Benjamin M. Nitsche ◽  
Pollyne Borborema Almeida de Lima ◽  
Leandro José de Assis ◽  
Laura Mellado ◽  
...  
Keyword(s):  
Aspergillus Nidulans ◽  
Glucose Transporter ◽  
Glucose Signalling

scholarly journals Expression of theHXT1Low Affinity Glucose Transporter Requires the Coordinated Activities of the HOG and Glucose Signalling Pathways

2004 ◽  
Vol 279 (21) ◽  
pp. 22010-22019 ◽  
Author(s):  
Lidia Tomás-Cobos ◽  
Laura Casadomé ◽  
Glòria Mas ◽  
Pascual Sanz ◽  
Francesc Posas
Keyword(s):  
Glucose Transporter ◽  
Signalling Pathways ◽  
Glucose Signalling

HIF1-α-Mediated Gene Expression Induced by Vitamin B1 Deficiency

2013 ◽  
Vol 83 (3) ◽  
pp. 188-197 ◽  
Author(s):  
Rebecca L. Sweet ◽  
Jason A. Zastre
Keyword(s):  
Gene Expression ◽  
Thiamine Deficiency ◽  
Glucose Transporter ◽  
Neuroblastoma Cell ◽  
Hypoxia Inducible Factor ◽  
Clinical Manifestations ◽  
Vitamin B1 ◽  
Low Oxygen ◽  
Glucose Transporter 1 ◽  
Metabolic Intermediates

It is well established that thiamine deficiency results in an excess of metabolic intermediates such as lactate and pyruvate, which is likely due to insufficient levels of cofactor for the function of thiamine-dependent enzymes. When in excess, both pyruvate and lactate can increase the stabilization of the hypoxia-inducible factor 1-alpha (HIF-1α) transcription factor, resulting in the trans-activation of HIF-1α regulated genes independent of low oxygen, termed pseudo-hypoxia. Therefore, the resulting dysfunction in cellular metabolism and accumulation of pyruvate and lactate during thiamine deficiency may facilitate a pseudo-hypoxic state. In order to investigate the possibility of a transcriptional relationship between hypoxia and thiamine deficiency, we measured alterations in metabolic intermediates, HIF-1α stabilization, and gene expression. We found an increase in intracellular pyruvate and extracellular lactate levels after thiamine deficiency exposure to the neuroblastoma cell line SK-N-BE. Similar to cells exposed to hypoxia, there was a corresponding increase in HIF-1α stabilization and activation of target gene expression during thiamine deficiency, including glucose transporter-1 (GLUT1), vascular endothelial growth factor (VEGF), and aldolase A. Both hypoxia and thiamine deficiency exposure resulted in an increase in the expression of the thiamine transporter SLC19A3. These results indicate thiamine deficiency induces HIF-1α-mediated gene expression similar to that observed in hypoxic stress, and may provide evidence for a central transcriptional response associated with the clinical manifestations of thiamine deficiency.

Glucose transporter isoform 1 (GLUT1) expression enhances formation and growth of hepatic metastases

2013 ◽  
Vol 51 (01) ◽  
Author(s):  
A Koch ◽  
P Wild ◽  
M Kreutz ◽  
A Bosserhoff ◽  
C Hellerbrand
Keyword(s):  
Glucose Transporter ◽  
Hepatic Metastases ◽  
Glut1 Expression

A Case of Congenital Glucose Galactose Malabsorption with a New Mutation in the SLC5A1 Gene

2020 ◽  
Author(s):  
Hasan Akduman ◽  
Dilek Dilli ◽  
Serdar Ceylaner
Keyword(s):  
Mutation Analysis ◽  
Autosomal Recessive ◽  
Glucose Transporter ◽  
Neonatal Period ◽  
Autosomal Recessive Disorder ◽  
Homozygous Mutation ◽  
New Mutation ◽  
Early Neonatal Period ◽  
Sodium Dependent ◽  
Hypernatremic Dehydration

AbstractCongenital glucose-galactose malabsorption (CGGM) is an autosomal recessive disorder originating from an abnormal transporter mechanism in the intestines. It was sourced from a mutation in the SLC5A1 gene, which encodes a sodium-dependent glucose transporter. Here we report a 2-day-old girl with CGGM who presented with severe hypernatremic dehydration due to diarrhea beginning in the first hours of life. Mutation analysis revealed a novel homozygous mutation NM_000343.3 c.127G > A (p.Gly43Arg) in the SLC5A1 gene. Since CGGM can cause fatal diarrhea in the early neonatal period, timely diagnosis of the disease seems to be essential.

503-P: Inhibition of Glucose Transporter 9 Increases Serum Uric Acid Level but Attenuates Renal Albumin Excretion in Streptozotocin-Induced Diabetic Rats: A Role of Hepatic Uric Acid Metabolism

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 503-P
Author(s):  
CHUPING CHEN ◽  
JIANMIN RAN ◽  
RUYI ZHANG ◽  
GUANGSHU CHEN ◽  
PING ZHU ◽  
...  
Keyword(s):  
Uric Acid ◽  
Serum Uric Acid ◽  
Uric Acid Level ◽  
Acid Level ◽  
Glucose Transporter ◽  
Acid Metabolism ◽  
Serum Uric Acid Level ◽  
Diabetic Rats ◽  
Glucose Transporter 9

Polymorphic human glucose transporter gene (GLUT) is on chromosome 1p31.3----p35

Diabetes ◽  
1987 ◽  
Vol 36 (4) ◽  
pp. 546-549 ◽  
Author(s):  
T. B. Shows ◽  
R. L. Eddy ◽  
M. G. Byers ◽  
Y. Fukushima ◽  
C. R. Dehaven ◽  
...  
Keyword(s):  
Glucose Transporter ◽  
Transporter Gene
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