The expression of glucose transporter isoforms (Glut 1, Glut 3, Glut 4, and Glut 5) in the human eye was investigated at various ages ranging between 8 weeks gestation (first trimester) and adult using Western blot and immunohistochemical analyses. Glut 1 and Glut 3 expression and cellular localization patterns were similar to those of human brain. Glut 1 (50-kilodalton protein) was expressed by epithelial cells (retinal pigmented epithelium, choroidal, iridial, and pars planus), which form the blood-eye barrier, retinal Mueller cells, the lens fiber cells, iridial microvascular endothelial cells, and to a lesser extent by the outer segments of the photoreceptor cells in the adult eye. This pattern was conserved throughout development and was evident as early as 8 weeks gestation. In addition, the endothelial cells of vitreous hyaloid vessels expressed Glut 1 at 8 weeks gestation. Glut 3 (50 to 55-kilodalton protein) immunoreactivity was observed only in the adult inner synaptic layer of the retina. Neither Glut 4 nor Glut 5 was expressed in any occular tissue at any age examined. These results suggest that Glut 1 is the main glucose transporter of the human eye and that it is ontogenically conserved. In contrast, Glut 3 is associated with selective neuronal processes, and its expression is developmentally altered.
In the present study we examined the expression and localization of Glut 3 in human brain using peptide-specific antisera. Glut 3 was expressed at 2-3 times higher levels in cerebral cortex from adult (n = 6) compared to that from neonatal infants (n = 4; P less than 0.05). However, similar levels of immunoreactive Glut 3 were present in cerebellum from adults (n = 6) and newborns (n = 4). Cellular localization of Glut 3 in adult (n = 5) and neonatal (n = 5) infant brains was undertaken by immunohistochemical analysis. Glut 3 was visible in the adult neuropil of the cerebral cortex; in certain cellular processes within the deeper cortical layers; in intravascular white cells, including monocytes, lymphocytes and granulocytes; and in microvascular endothelial cells. Neither the premature nor the mature newborn cerebral cortex exhibited Glut 3 labeling in the neuropil or microvasculature. In the cerebellum, given the stratified nature of the cellular arrangement, Glut 3 was more clearly and definitively noted in the cellular processes at all stages of development. Double labeling studies using neuronal (neurofilament) and astrocytic (glial fibrillary acidic protein) markers indicated that Glut 3 was primarily expressed in neurons. We conclude that Glut 3 is localized in many cellular components, including white blood cells in human brain. The prominent localization of Glut 3 to mature neuronal processes suggests an essential role for this transporter in regulating fuel requirements for dendritic and axonal traffic, thereby mediating neurotransmission. Further study is required to address the possibility that another as yet undefined glucose transporter isoform is expressed in other cell-specific regions of the brain.
Objective: To determine whether earlier treatment of high-risk, prethreshold retinopathy of prematurity (ROP) improves retinal structural outcome at 2 years of age. Methods: Infants with bilateral high-risk prethreshold ROP had one eye randomly assigned to treatment with peripheral retinal ablation. The fellow eye was managed conventionally, and either treated at threshold ROP or observed if threshold was never reached. In patients with asymmetrical disease, the highrisk, prethreshold eye was randomised to earlier treatment or to conventional management. At 2 years of age, children were examined comprehensively by certified ophthalmologists to determine structural outcomes for their eyes. For the purposes of this study, an unfavourable structural outcome was defined as (1) a posterior retinal fold involving the macula, (2) a retinal detachment involving the macula or (3) retrolental tissue or ''mass'' obscuring the view of the posterior pole. Results of the 2-year examination were compared with those from the 9 months examination. Results: Data were available on 339 of 374 (90.6%) surviving children. Unfavourable structural outcomes were reduced from 15.4% in conventionally managed eyes to 9.1% in earlier-treated eyes (p = 0.002) at 2 years of age. Ophthalmic side effects (excluding retinal structure) from the ROP or its treatment were similar in the earlier-treated eyes and the conventionally managed eyes. Conclusion:The benefit of earlier treatment of high-risk prethreshold ROP on retinal structure endures to 2 years of age, and is not counterbalanced by any known side effect caused by earlier intervention. Earlier treatment improves the chance for long-term favourable retinal structural outcome in eyes with high-risk prethreshold ROP. Long-term follow-up is planned to determine structural and functional outcomes at 6 years of age.T he Early Treatment for Retinopathy Of Prematurity (ETROP) Study showed that retinal ablation for highrisk prethreshold retinopathy of prematurity (ROP) improved structural and functional outcomes, compared with conventional management, when infants were examined at 9 months' corrected age. 1 The study randomised infants who had both prethreshold disease and a risk for unfavourable structural outcome >15%. 2However, eyes of infants may change over time.3 Myopia, strabismus and late retinal detachments all increase in frequency in the months and years after successful treatment of ROP.3 4 In the Cryotherapy for Retinopathy of Prematurity (CRYO-ROP) Study, a wide distribution of optotype acuities developed after successful treatment, with 75% showing acuities worse than 20/40 when children reached 10 and 15 years of age.3 5 Time will tell whether the ETROP cohort will show the same distribution of functional outcomes as occurred in the CRYO-ROP Study.In the CRYO-ROP Study, only a few infants had threshold disease in zone I, 6 but in the ETROP Study, 40% of all randomised children had zone I disease. This group of children may be particularly vulnerable to complications of myopia, stra...
The recently cloned Glut-5, glucose transporter isoform, is expressed in human jejunum and kidney. Employing previously characterized polyclonal antibodies directed towards the C-terminus region of the derived human Glut-5 peptide and Western blot analysis, a 50-55 kilodalton Glut-5 protein was detected in adult human brain homogenates. The amount of Glut-5 protein in brain was 4-fold lower when compared to the levels in adult kidney. Immunohistochemical analysis using cerebral and cerebellar sections demonstrated Glut-5 immunoreactivity in only some of the Glut-1 and factor VIII-positive brain microvascular endothelial cells, the intravascular red and white blood cells being negative. This selective localization pattern was confirmed by the 5-fold enrichment of Glut-5 vs. a 20-fold enrichment of Glut-1 in an isolated human cerebral cortical microvascular preparation, when compared to whole cerebral homogenates. We conclude that Glut-5 is localized in the endothelial cells of human brain microvasculature. Unlike other fructose using tissues, where Glut-5 may subserve the role of a fructose carrier, in brain where fructose is not used as a substrate, Glut-5 may transport glucose alone. This role of Glut-5 in conjunction with the previously characterized brain endothelial Glut-1 and Glut-3 needs further elucidation.
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