Glucose Transport Stimulation by Thyroid Hormone in ARL 15 Cells: Partial Role of Increased GLUT1 Glucose Transporter Gene Transcription

Thyroid ◽  
1993 ◽  
Vol 3 (2) ◽  
pp. 135-142 ◽  
Author(s):  
STEVEN P. WEINSTEIN ◽  
RICHARD S. HABER
Keyword(s):  
Thyroid Hormone ◽  
Glucose Transport ◽  
Gene Transcription ◽  
Glucose Transporter ◽  
Transporter Gene ◽  
Glut1 Glucose Transporter

GLUT1 glucose transporter gene transcription is repressed by Sp3. Evidence for a regulatory role of Sp3 during myogenesis 1 1Edited by M. Yaniv

1999 ◽  
Vol 294 (1) ◽  
pp. 103-119 ◽  
Author(s):  
César Fandos ◽  
Manuela Sánchez-Feutrie ◽  
Tomàs Santalucı́a ◽  
Francesc Viñals ◽  
Joan Cadefau ◽  
...  
Keyword(s):  
Gene Transcription ◽  
Glucose Transporter ◽  
Regulatory Role ◽  
Transporter Gene ◽  
Glut1 Glucose Transporter

scholarly journals Essential role of glucose transporter GLUT3 for post-implantation embryonic development

2008 ◽  
Vol 200 (1) ◽  
pp. 23-33 ◽  
Author(s):  
S Schmidt ◽  
A Hommel ◽  
V Gawlik ◽  
R Augustin ◽  
N Junicke ◽  
...  
Keyword(s):  
Essential Role ◽  
Glucose Transporter ◽  
Growth Arrest ◽  
Complete Loss ◽  
Transporter Gene ◽  
Wild Type ◽  
Post Implantation ◽  
Time Point

Deletion of glucose transporter geneSlc2a3(GLUT3) has previously been reported to result in embryonic lethality. Here, we define the exact time point of growth arrest and subsequent death of the embryo.Slc2a3−/−morulae and blastocysts developed normally, implantedin vivo, and formed egg-cylinder-stage embryos that appeared normal until day 6.0. At day 6.5, apoptosis was detected in the ectodermal cells ofSlc2a3−/−embryos resulting in severe disorganization and growth retardation at day 7.5 and complete loss of embryos at day 12.5. GLUT3 was detected in placental cone, in the visceral ectoderm and in the mesoderm of 7.5-day-old wild-type embryos. Our data indicate that GLUT3 is essential for the development of early post-implanted embryos.

scholarly journals Lactose-over-Glucose Preference in Bifidobacterium longum NCC2705: glcP, Encoding a Glucose Transporter, Is Subject to Lactose Repression

2006 ◽  
Vol 188 (4) ◽  
pp. 1260-1265 ◽  
Author(s):  
Stephan Parche ◽  
Manfred Beleut ◽  
Enea Rezzonico ◽  
Doris Jacobs ◽  
Fabrizio Arigoni ◽  
...  
Keyword(s):  
Glucose Transport ◽  
Culture Medium ◽  
Glucose Transporter ◽  
Glucose Utilization ◽  
Bifidobacterium Longum ◽  
Global Gene Expression ◽  
Dna Arrays ◽  
Transporter Gene ◽  
Global Gene Expression Profiling ◽  
Culture Supernatants

ABSTRACT Analysis of culture supernatants obtained from Bifidobacterium longum NCC2705 grown on glucose and lactose revealed that glucose utilization is impaired until depletion of lactose. Thus, unlike many other bacteria, B. longum preferentially uses lactose rather than glucose as the primary carbon source. Glucose uptake experiments with B. longum cells showed that glucose transport was repressed in the presence of lactose. A comparative analysis of global gene expression profiling using DNA arrays led to the identification of only one gene repressed by lactose, the putative glucose transporter gene glcP. The functionality of GlcP as glucose transporter was demonstrated by heterologous complementation of a glucose transport-deficient Escherichia coli strain. Additionally, GlcP exhibited the highest substrate specificity for glucose. Primer extension and real-time PCR analyses confirmed that expression of glcP was mediated by lactose. Hence, our data demonstrate that the presence of lactose in culture medium leads to the repression of glucose transport and transcriptional down-regulation of the glucose transporter gene glcP. This may reflect the highly adapted life-style of B. longum in the gastrointestinal tract of mammals.

Stimulation of GLUT-1 glucose transporter expression in response to exposure to calcium ionophore A-23187

1995 ◽  
Vol 269 (5) ◽  
pp. C1228-C1234 ◽  
Author(s):  
Y. Mitani ◽  
A. Behrooz ◽  
G. R. Dubyak ◽  
F. Ismail-Beigi
Keyword(s):  
Gene Expression ◽  
Glucose Transport ◽  
Gene Transcription ◽  
Glucose Transporter ◽  
Calcium Ionophore ◽  
Tetraacetic Acid ◽  
Glut 1 ◽  
Mrna Induction ◽  
A 23187 ◽  
Mrna Content

We tested the hypothesis that an increase in cytosolic calcium concentration stimulates glucose transporter isoform (GLUT-1) gene expression. Exposure of a rat liver cell line (Clone 9) to 3 microM A-23187 for 12 h resulted in 3-, 5-, and 10-fold increases in cytochalasin B-inhibitable 3-O-methyl-D-glucose transport, GLUT-1 protein, and GLUT-1 mRNA content, respectively. The induction of GLUT-1 mRNA in response to A-23187 is not preceded by a significant decrease in cell ATP content. This induction is prevented by 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid in conjunction with ethylene glycol-bis(beta-aminoethyl ether)-N,N, N',N'-tetraacetic acid. To investigate the mechanism of GLUT-1 mRNA induction, we found that exposure to A-23187 stabilized GLUT-1 mRNA: with the employment of actinomycin D, GLUT-1 mRNA had a half-life of 1.5 and 5.5 h in control and A-23187-treated cells, respectively. In nuclear run-on assays, the rate of GLUT-1 gene transcription was stimulated 1.5- to 1.7-fold in nuclei isolated from cells exposed to A-23187 for either 30 min or 2 h. These results demonstrate that exposure to A-23187 stimulates GLUT-1 gene expression and that the increase in GLUT-1 mRNA content is mediated in part by enhanced GLUT-1 gene transcription as well as decreased GLUT-1 mRNA degradation. The increase in GLUT-1 mRNA content, in turn, is associated with increased cell GLUT-1 content and enhanced glucose transport.

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