Disease relevance of Slc2a3

• 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 [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].
• It is concluded that 1 week of hypoglycemia is a stimulus for the induction of additional glucose transporters Glut3 in the brain [3].
• Degenerative changes in spermatogonia are associated with loss of glucose transporter (Glut 3) in abdominal testis of surgically induced unilateral cryptorchidism in rats [4].
• In addition, IUGR caused a approximately 45% increase in fetal brain Glut 1 (55 kDa) with no change in Glut 3 (50 kDa) protein concentrations [5].

Psychiatry related information on Slc2a3

• 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 Slc2a3

• 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].
• Glucose transporter Glut3 is targeted to secretory vesicles in neurons and PC12 cells [8].
• Glut3-containing vesicles co-purify with "classical" synaptic vesicles, but can be separated from the latter by sucrose gradient centrifugation [8].
• The expression levels of Glut-1, Glut-3, and HK-II were determined by immunostaining and semiquantitative evaluation [2].
• Neither Glut 3 nor Glut 4 mRNA could be detected in STZ-treated and control fetal muscle [9].

Chemical compound and disease context of Slc2a3

• Effects of gestational hypoxia on mRNA levels of Glut3 and Glut4 transporters, hypoxia inducible factor-1 and thyroid hormone receptors in developing rat brain [10].

Biological context of Slc2a3

• 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 [1].
• Ethanol-induced decrease of the expression of glucose transport protein (Glut3) in the central nervous system as a predisposing condition to apoptosis: the effect of age [11].
• Molecular probing throughout a simulated estrous cycle revealed a significant surge in ovarian Glut3 (but not Glut1) expression at the time of ovulation [7].
• To examine the effect of excessive circulating glucose on fetal brain glucose transporter expression, we investigated the effect of streptozotocin-induced maternal diabetes (SEVERE-D; n = 29) on the 20-d gestation fetal rat brain Glut 1 and Glut 3 [12].
• Immunohistochemistry of Glut3 (45 kD), an integral membrane peptide mediating the transport of glucose in neurons, was carried out in the hippocampus of 3- and 28-month-old rats to assess the effect of age on energy metabolism [13].

Anatomical context of Slc2a3

• Glut1 is expressed in endothelial cells of the blood-brain barrier (BBB) and also in glia, while Glut3 is the primary glucose transporter expressed in neurons [1].
• The increase in Glut3 expression was clearly evident in both the cerebral cortex and cerebellum [1].
• We measured the effect of chronic ethanol administration on the expression of Glut3 in the cerebellum and hippocampus of adult and old rats [11].
• Glut 3 expression was reduced by 85-95% compared with contralateral scrotal testis [4].
• The abundance of Glut3 in cerebrum of Co(II)-treated rats also increased by 1.3-fold (P<0. 05), but the increase was not associated with a change in the content of Glut3 mRNA [14].

Associations of Slc2a3 with chemical compounds

• Increase of glucose transporter densities (Glut1 and Glut3) during chronic administration of nicotine in rat brain [15].
• To determine whether the increased density of Glut3 is related to a change in glucose metabolism, the local cerebral metabolic rate of glucose (lCMR(glc)) was quantified by the 2-deoxyglucose method [3].
• 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 [16].

Regulatory relationships of Slc2a3

• Glut 3 mRNA levels in STZ-treated and control fetal brain were equivalent and significantly less than levels of Glut 1 [9].

Other interactions of Slc2a3

• 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].

Analytical, diagnostic and therapeutic context of Slc2a3

• Free-floating sections of fixed-frozen hippocampi were processed for quantitative immunohistochemistry of Glut3 [13].
• This study is realised in rats by quantification of whole brain Glut3 and Glut4 mRNA in 14- and 19-day-old embryos (E14, E19), newborn (P0) and 7 postnatal-day-old rats (P7) by using reverse transcription-polymerase chain reaction (RT-PCR) method [10].

References