Disease relevance of Slc2a1

• Thus, Ras activation and pathways downstream of Ras mediate induction of the Glut1 promoter during myocardial hypertrophy [1].
• The elevated expression levels of Glut-1, Glut-3, and HK-II, induced by hypoxia (HIF-1), may be contributing factors to the higher 18F-FDG accumulation in the CT region [2].
• We conclude that maternal diabetes causing fetal hyperglycemia with normoinsulinemia suppresses fetal myocardial Glut 1 and Glut 4 and fetal skeletal muscle Glut 1 [3].
• IUGR increased the fetal hepatic Glut 1 levels in parallel with an expanded hematopoietic cell mass (p < 0.05) [4].
• This study has therefore focussed on investigating the expression of the glial specific 45-kDa isoform of Glut1 and neuronal specific Glut3 following severe diffuse traumatic brain injury in rats [5].

Psychiatry related information on Slc2a1

• After 3 days of water deprivation, the following parameters were measured in rats: (i) brain water content (apparent diffusion coefficient); (ii) local cerebral glucose utilization (LCGU) ([14C]deoxyglucose method) and (iii) densities of glucose transporters Glut1 and Glut3 (immunoautoradiography) [6].

High impact information on Slc2a1

• Treatment of cultured whole ovarian dispersates from immature rats with IL-1beta resulted in upregulation of the relative abundance of the Glut1 (4.5-fold) and Glut3 (3.5-fold) proteins as determined by Western blot analysis [7].
• Divergent regulation of the Glut 1 and Glut 4 glucose transporters in isolated adipocytes from Zucker rats [8].
• Basal glucose uptake is increased severalfold in fat cells from obese rats, and in parallel Glut 1 expression per cell in obese rats is two- to threefold increased over lean rats at all ages [8].
• We have studied the relationship between glucose uptake rate and Glut 1 and Glut 4 protein and mRNA levels per fat cell in lean (FA/FA) and obese (fa/fa) Zucker rats at 5, 10, and 20 wk of age, and after induction of acute diabetes with streptozotocin [8].
• The protective potential of such a vector was tested by inclusion of a neuroprotective transgene (the Glut-1 glucose transporter) [9].

Chemical compound and disease context of Slc2a1

• The results are consistent with the hypothesis that sepsis enhances glucose uptake secondary to increased Glut-1 expression [10].

Biological context of Slc2a1

• Molecular probing throughout a simulated estrous cycle revealed a significant surge in ovarian Glut3 (but not Glut1) expression at the time of ovulation [7].
• Acute diabetes in 20 wk obese rats causes a profound downregulation of glucose uptake and a concomitant reduction of both Glut 1 and Glut 4 protein levels [8].
• H-raslys12-transformed brown adipocytes showed a 10-fold higher expression of Glut1 mRNA and protein than parental cells, Glut4 gene expression being completely down-regulated [11].
• These data support the conclusion that the prolonged increase in glucose transport rate is due to either the transcriptional activation of Glut1 and/or the increased Glut1 mRNA half-life [12].
• Increased glycolysis must be met by increasing glucose supply that, in brain, is primarily mediated by two members of the facilitative glucose transporter family, Glut1 and Glut3 [5].

Anatomical context of Slc2a1

• To study the transcriptional regulation of GLUT1 expression, myocytes were transfected with luciferase reporter constructs under the control of the Glut1 promoter [1].
• The t1/2 values for ER to Golgi transit for Glut1 and Glut4 were < 1 and 24 h, respectively, in oocytes and approximately 5 and 20 min, respectively, in 3T3-L1 adipocytes [13].
• Treatment of neonatal cardiac myocytes with the hypertrophic agonist 12-O-tetradecanoylphorbol-13-acetate or phenylephrine increased expression of Glut1 mRNA relative to Glut4 mRNA [1].
• Glucose transport in skeletal muscle is mediated by two distinct transporter isoforms, designated muscle/adipose glucose transporter (Glut4) and erythrocyte/HepG2/brain glucose transporter (Glut1), which differ in both abundance and membrane distribution [14].
• In the lactating mammary gland only Glut 1 was present, and was expressed at a high level [15].

Associations of Slc2a1 with chemical compounds

• We previously identified (Hwang DY and Ismail-Beigi F. Am J Physiol Cell Physiol 281: C1365-C1372, 2001) a 44-bp GC-rich segment of the rat proximal glucose transporter (Glut)1 promoter, located at -104 to -61, as necessary for basal transcription of the Glut1 gene [16].
• Exposure of cells to trichostatin A resulted in increased expression of the endogenous Glut1 as well as the transfected wild-type construct [16].
• Glut1 and glut3 expression, but not capillary density, is increased by cobalt chloride in rat cerebrum and retina [17].
• Increase of glucose transporter densities (Glut1 and Glut3) during chronic administration of nicotine in rat brain [18].
• We suggest that those regional effects are explained, at least for a part, by the fact that central isoform glucose transporters (Glut1 and Glut3) are known to be more sensitive to pentobarbital than peripheral isoforms [19].

Regulatory relationships of Slc2a1

• Cotransfection of the myocytes with constitutively active versions of Ras and MEK1 or an estrogen-inducible version of Raf1 also stimulated transcription from the Glut1 promoter [1].
• Glut 3 mRNA levels in STZ-treated and control fetal brain were equivalent and significantly less than levels of Glut 1 [20].
• These observations suggest that changes in basal and IGF-I-stimulated Glut-1 system in brain astrocytes may be developmentally regulated [21].

Other interactions of Slc2a1

• Control of Glut1 promoter activity under basal conditions and in response to hyperosmolarity: role of Sp1 [16].
• To examine the role of the exofacial cysteine, we replaced Met-455 of Glut4 (corresponding to Cys-429 of Glut1) with cysteine [22].
• We conclude that hepatic Glut 1 concentrations reflect the extramedullary hematopoietic cellular mass, whereas extrauterine Glut 2 changes herald the need for enhanced flexibility in hepatocytic glucose transport with the initiation of food ingestion [4].
• Using firefly luciferase as reporter gene, additional experiments showed that IGF-1 activated the promoter of cyclin D3 and Glut1 [23].
• CONCLUSION: These results demonstrate that intratumoral 18F-FDG distribution corresponds well to the expression levels of Glut-1, Glut-3, and HK-II [2].

Analytical, diagnostic and therapeutic context of Slc2a1

• To clarify factors inducing heterogeneous 18F-FDG distribution, we determined the intratumoral distribution of 18F-FDG by autoradiography (ARG) and compared it with the regional expression levels of glucose transporters Glut-1 and Glut-3 and hexokinase-II (HK-II) in a rat model of malignant tumor [2].
• Simultaneous measurement of multiple mRNAs with a single control by quantitative competitive reverse transcriptase-polymerase chain reaction: glucose transporters Glut1 and Glut4 [24].
• This PCR system was able to reliably detect differences as little as 50% in the initial concentration of the Glut1 target DNA sequence [24].
• The increase in Glut1 content was associated with a significant increase in the content of Glut1 staining in microvessels isolated from cerebral gray matter, and in the intensity of Glut1 in microvessels of the frontal lobe and hippocampus assessed by immunohistochemistry [17].
• These alterations in Glut isoforms after denervation may be associated with the removal of innervation itself, and/or may partly result from passive stretch imposed by inspiratory activation of the contralateral side [25].

References