Glucose transporter protein expression in human placenta throughout gestation and in intrauterine growth retardation.

@article{Jansson1993GlucoseTP,
  title={Glucose transporter protein expression in human placenta throughout gestation and in intrauterine growth retardation.},
  author={T. Jansson and Margareta M Wennergren and Nicholas P. Illsley},
  journal={The Journal of clinical endocrinology and metabolism},
  year={1993},
  volume={77 6},
  pages={1554-62}
}
Despite the importance of glucose for fetal growth, gestational development of placental glucose transport capacity has not been studied in the human. Furthermore, inadequate glucose transport has been implicated as a pathophysiological mechanism in intrauterine growth retardation (IUGR). We studied glucose transporter (GLUT) protein expression in sections of normal term placental tissue (immunocytochemistry) and in syncytiotrophoblast microvillous (MVM) and basal membranes (BM) isolated from… CONTINUE READING
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These data suggest that 1 ) GLUT 1 is the main glucose transporter protein isoform in human syncytiotrophoblast ; 2 ) the glucose transport capacity for MVM is potentially approximately 20-fold higher than that of BM ; 3 ) GLUT 1 densities may be regulated independently in MVM and BM ; 4 ) the increase in surface area and the maintenance of a high GLUT 1 density can account for the increase in placental glucose transport in the latter part of pregnancy ; and 5 ) fetal hypoglycemia in IUGR is not due to a decrease in placental glucose transporter density .
These data suggest that 1 ) GLUT 1 is the main glucose transporter protein isoform in human syncytiotrophoblast ; 2 ) the glucose transport capacity for MVM is potentially approximately 20-fold higher than that of BM ; 3 ) GLUT 1 densities may be regulated independently in MVM and BM ; 4 ) the increase in surface area and the maintenance of a high GLUT 1 density can account for the increase in placental glucose transport in the latter part of pregnancy ; and 5 ) fetal hypoglycemia in IUGR is not due to a decrease in placental glucose transporter density .
These data suggest that 1 ) GLUT 1 is the main glucose transporter protein isoform in human syncytiotrophoblast ; 2 ) the glucose transport capacity for MVM is potentially approximately 20-fold higher than that of BM ; 3 ) GLUT 1 densities may be regulated independently in MVM and BM ; 4 ) the increase in surface area and the maintenance of a high GLUT 1 density can account for the increase in placental glucose transport in the latter part of pregnancy ; and 5 ) fetal hypoglycemia in IUGR is not due to a decrease in placental glucose transporter density .
These data suggest that 1 ) GLUT 1 is the main glucose transporter protein isoform in human syncytiotrophoblast ; 2 ) the glucose transport capacity for MVM is potentially approximately 20-fold higher than that of BM ; 3 ) GLUT 1 densities may be regulated independently in MVM and BM ; 4 ) the increase in surface area and the maintenance of a high GLUT 1 density can account for the increase in placental glucose transport in the latter part of pregnancy ; and 5 ) fetal hypoglycemia in IUGR is not due to a decrease in placental glucose transporter density .
We studied glucose transporter ( GLUT ) protein expression in sections of normal term placental tissue ( immunocytochemistry ) and in syncytiotrophoblast microvillous ( MVM ) and basal membranes ( BM ) isolated from normal term , preterm , and IUGR placentas ( immunoblotting ) .
We studied glucose transporter ( GLUT ) protein expression in sections of normal term placental tissue ( immunocytochemistry ) and in syncytiotrophoblast microvillous ( MVM ) and basal membranes ( BM ) isolated from normal term , preterm , and IUGR placentas ( immunoblotting ) .
These data suggest that 1 ) GLUT 1 is the main glucose transporter protein isoform in human syncytiotrophoblast ; 2 ) the glucose transport capacity for MVM is potentially approximately 20-fold higher than that of BM ; 3 ) GLUT 1 densities may be regulated independently in MVM and BM ; 4 ) the increase in surface area and the maintenance of a high GLUT 1 density can account for the increase in placental glucose transport in the latter part of pregnancy ; and 5 ) fetal hypoglycemia in IUGR is not due to a decrease in placental glucose transporter density .
These data suggest that 1 ) GLUT 1 is the main glucose transporter protein isoform in human syncytiotrophoblast ; 2 ) the glucose transport capacity for MVM is potentially approximately 20-fold higher than that of BM ; 3 ) GLUT 1 densities may be regulated independently in MVM and BM ; 4 ) the increase in surface area and the maintenance of a high GLUT 1 density can account for the increase in placental glucose transport in the latter part of pregnancy ; and 5 ) fetal hypoglycemia in IUGR is not due to a decrease in placental glucose transporter density .
We studied glucose transporter ( GLUT ) protein expression in sections of normal term placental tissue ( immunocytochemistry ) and in syncytiotrophoblast microvillous ( MVM ) and basal membranes ( BM ) isolated from normal term , preterm , and IUGR placentas ( immunoblotting ) .
We studied glucose transporter ( GLUT ) protein expression in sections of normal term placental tissue ( immunocytochemistry ) and in syncytiotrophoblast microvillous ( MVM ) and basal membranes ( BM ) isolated from normal term , preterm , and IUGR placentas ( immunoblotting ) .
These data suggest that 1 ) GLUT 1 is the main glucose transporter protein isoform in human syncytiotrophoblast ; 2 ) the glucose transport capacity for MVM is potentially approximately 20-fold higher than that of BM ; 3 ) GLUT 1 densities may be regulated independently in MVM and BM ; 4 ) the increase in surface area and the maintenance of a high GLUT 1 density can account for the increase in placental glucose transport in the latter part of pregnancy ; and 5 ) fetal hypoglycemia in IUGR is not due to a decrease in placental glucose transporter density .
These data suggest that 1 ) GLUT 1 is the main glucose transporter protein isoform in human syncytiotrophoblast ; 2 ) the glucose transport capacity for MVM is potentially approximately 20-fold higher than that of BM ; 3 ) GLUT 1 densities may be regulated independently in MVM and BM ; 4 ) the increase in surface area and the maintenance of a high GLUT 1 density can account for the increase in placental glucose transport in the latter part of pregnancy ; and 5 ) fetal hypoglycemia in IUGR is not due to a decrease in placental glucose transporter density .
These data suggest that 1 ) GLUT 1 is the main glucose transporter protein isoform in human syncytiotrophoblast ; 2 ) the glucose transport capacity for MVM is potentially approximately 20-fold higher than that of BM ; 3 ) GLUT 1 densities may be regulated independently in MVM and BM ; 4 ) the increase in surface area and the maintenance of a high GLUT 1 density can account for the increase in placental glucose transport in the latter part of pregnancy ; and 5 ) fetal hypoglycemia in IUGR is not due to a decrease in placental glucose transporter density .
These data suggest that 1 ) GLUT 1 is the main glucose transporter protein isoform in human syncytiotrophoblast ; 2 ) the glucose transport capacity for MVM is potentially approximately 20-fold higher than that of BM ; 3 ) GLUT 1 densities may be regulated independently in MVM and BM ; 4 ) the increase in surface area and the maintenance of a high GLUT 1 density can account for the increase in placental glucose transport in the latter part of pregnancy ; and 5 ) fetal hypoglycemia in IUGR is not due to a decrease in placental glucose transporter density .
These data suggest that 1 ) GLUT 1 is the main glucose transporter protein isoform in human syncytiotrophoblast ; 2 ) the glucose transport capacity for MVM is potentially approximately 20-fold higher than that of BM ; 3 ) GLUT 1 densities may be regulated independently in MVM and BM ; 4 ) the increase in surface area and the maintenance of a high GLUT 1 density can account for the increase in placental glucose transport in the latter part of pregnancy ; and 5 ) fetal hypoglycemia in IUGR is not due to a decrease in placental glucose transporter density .
These data suggest that 1 ) GLUT 1 is the main glucose transporter protein isoform in human syncytiotrophoblast ; 2 ) the glucose transport capacity for MVM is potentially approximately 20-fold higher than that of BM ; 3 ) GLUT 1 densities may be regulated independently in MVM and BM ; 4 ) the increase in surface area and the maintenance of a high GLUT 1 density can account for the increase in placental glucose transport in the latter part of pregnancy ; and 5 ) fetal hypoglycemia in IUGR is not due to a decrease in placental glucose transporter density .
GLUT 1 , but not GLUT 3 , protein was abundantly present in syncytiotrophoblast membranes .
These data suggest that 1 ) GLUT 1 is the main glucose transporter protein isoform in human syncytiotrophoblast ; 2 ) the glucose transport capacity for MVM is potentially approximately 20-fold higher than that of BM ; 3 ) GLUT 1 densities may be regulated independently in MVM and BM ; 4 ) the increase in surface area and the maintenance of a high GLUT 1 density can account for the increase in placental glucose transport in the latter part of pregnancy ; and 5 ) fetal hypoglycemia in IUGR is not due to a decrease in placental glucose transporter density .
These data suggest that 1 ) GLUT 1 is the main glucose transporter protein isoform in human syncytiotrophoblast ; 2 ) the glucose transport capacity for MVM is potentially approximately 20-fold higher than that of BM ; 3 ) GLUT 1 densities may be regulated independently in MVM and BM ; 4 ) the increase in surface area and the maintenance of a high GLUT 1 density can account for the increase in placental glucose transport in the latter part of pregnancy ; and 5 ) fetal hypoglycemia in IUGR is not due to a decrease in placental glucose transporter density .
These data suggest that 1 ) GLUT 1 is the main glucose transporter protein isoform in human syncytiotrophoblast ; 2 ) the glucose transport capacity for MVM is potentially approximately 20-fold higher than that of BM ; 3 ) GLUT 1 densities may be regulated independently in MVM and BM ; 4 ) the increase in surface area and the maintenance of a high GLUT 1 density can account for the increase in placental glucose transport in the latter part of pregnancy ; and 5 ) fetal hypoglycemia in IUGR is not due to a decrease in placental glucose transporter density .
These data suggest that 1 ) GLUT 1 is the main glucose transporter protein isoform in human syncytiotrophoblast ; 2 ) the glucose transport capacity for MVM is potentially approximately 20-fold higher than that of BM ; 3 ) GLUT 1 densities may be regulated independently in MVM and BM ; 4 ) the increase in surface area and the maintenance of a high GLUT 1 density can account for the increase in placental glucose transport in the latter part of pregnancy ; and 5 ) fetal hypoglycemia in IUGR is not due to a decrease in placental glucose transporter density .
GLUT 1 , but not GLUT 3 , protein was abundantly present in syncytiotrophoblast membranes .
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