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The blood-brain barrier glucose transporter is conserved in preterm and term newborn infants
G J Mantych1, C Sotelo-Avila, S U Devaskar
1Divisions of Neonatology, St. Louis University School of Medicine, Missouri.
Insights
Glucose transporter Glut 1 is present in newborn brains at levels comparable to adults. This finding is crucial for detecting and treating defective glucose transport in infants, potentially preventing neurological damage.
Area of Science:
- Neuroscience
- Biochemistry
- Developmental Biology
Background:
- Glucose is vital for brain energy metabolism.
- The blood-brain barrier regulates nutrient transport into the brain.
- Glut 1 (glucose transporter 1) facilitates glucose passage across the blood-brain barrier in adults.
Purpose of the Study:
- To investigate the presence and levels of Glut 1 in the neonatal blood-brain barrier.
- To determine if Glut 1 expression is conserved from neonates to adults.
- To establish the feasibility of detecting neonatal glucose transport defects.
Main Methods:
- Western blot analysis of postmortem human brain samples.
- Immunohistochemical analysis of paraffin-embedded infant and adult brain sections.
Main Results:
- Glut 1 protein (47-55 kDa) was detected in both preterm and term neonates.
- Neonatal Glut 1 levels were comparable to adult levels.
- Glut 1 was localized to microvascular endothelial cells of the blood-brain barrier in neonates, similar to adults.
Conclusions:
- The blood-brain barrier's Glut 1 transporter is conserved throughout development.
- This conservation allows for the detection of impaired glucose transport in newborns.
- Early identification of Glut 1 defects can lead to interventions, potentially improving neurological outcomes in affected infants.
Abstract:
Glucose, an essential substrate for brain oxidative metabolism, is transported across the adult blood-brain barrier by Glut 1, a facilitative glucose transporter. Employing postmortem human brain samples and Western blot analysis, we demonstrated the presence of a 47-55 kilodalton Glut 1 protein in preterm and term newborn. The level of Glut 1 in both the preterm (24-33 weeks; n = 12) and term (38-40 weeks; n = 4) neonates was comparable to that of the adult (n = 5). Using paraffin brain sections and immunohistochemical analysis, in the preterm (24-25 weeks) and term (40 weeks) infant, similar to the adult we demonstrated the presence of Glut 1 in microvascular endothelial cells which constitute blood-brain barrier forming cells. The ontogenic conservation of the blood-brain barrier Glut 1 make detecting defective glucose transport across the neonatal blood-brain barrier feasible. Genetic or acquired defects in Glut 1 can impede the transport of glucose across the blood-brain barrier, thereby, resulting in irreversible neurological compromise during infancy. Earlier detection during the neonatal period, and appropriate intervention, may set the stage for altering the outcome of affected infants.