THE BLOOD-BRAIN-BARRIER GLUCOSE-TRANSPORTER IS CONSERVED IN PRETERM AND TERM NEWBORN-INFANTS

被引:16
作者
MANTYCH, GJ
SOTELOAVILA, C
DEVASKAR, SU
机构
[1] PEDIAT RES INST, 3662 PK AVE, ST LOUIS, MO 63110 USA
[2] ST LOUIS UNIV, SCH MED, DEPT PEDIAT, DIV NEONATOL, ST LOUIS, MO 63104 USA
[3] ST LOUIS UNIV, SCH MED, DEPT PEDIAT, DIV CELL & DEV BIOL, ST LOUIS, MO 63104 USA
[4] ST LOUIS UNIV, SCH MED, DEPT PATHOL, ST LOUIS, MO 63104 USA
[5] CARDINAL GLENNON MEM HOSP CHILDREN, ST LOUIS, MO 63104 USA
关键词
D O I
10.1210/jc.77.1.46
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 makes 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.
引用
收藏
页码:46 / 49
页数:4
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