Blood-brain transfer of galactose in experimental galactosemia, with special reference to the competitive interaction between galactose and glucose.

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Blood-brain transfer of galactose in experimental galactosemia, with special reference to the competitive interaction between galactose and glucose. / Gjedde, A.

In: Journal of Neurochemistry, Vol. 43, No. 6, 1984, p. 1654-62.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Gjedde, A 1984, 'Blood-brain transfer of galactose in experimental galactosemia, with special reference to the competitive interaction between galactose and glucose.', Journal of Neurochemistry, vol. 43, no. 6, pp. 1654-62.

APA

Gjedde, A. (1984). Blood-brain transfer of galactose in experimental galactosemia, with special reference to the competitive interaction between galactose and glucose. Journal of Neurochemistry, 43(6), 1654-62.

Vancouver

Gjedde A. Blood-brain transfer of galactose in experimental galactosemia, with special reference to the competitive interaction between galactose and glucose. Journal of Neurochemistry. 1984;43(6):1654-62.

Author

Gjedde, A. / Blood-brain transfer of galactose in experimental galactosemia, with special reference to the competitive interaction between galactose and glucose. In: Journal of Neurochemistry. 1984 ; Vol. 43, No. 6. pp. 1654-62.

Bibtex

@article{35617c80b31511debc73000ea68e967b,
title = "Blood-brain transfer of galactose in experimental galactosemia, with special reference to the competitive interaction between galactose and glucose.",
abstract = "The interaction between glucose and galactose during transport across the cerebral capillary endothelium was studied in anesthetized rats. Although galactose is present in the diet of suckling mammals and is a potential substrate for brain metabolism in adult mammals, its effect on glucose transport in adult rats is unknown. A kinetic model was formulated to analyze the effect of chronically elevated galactose levels on glucose transport in adult rats. The analysis indicated that galactose and glucose compete for the same transport mechanism in the cerebral capillary endothelium. The Tmax of glucose and galactose were both about 380 mumol 100 g-1 min-1 and the Kt of galactose (30 mM) was about three times that of glucose (10 mM). During prolonged galactosemia in adult rats, neither the Tmax, nor the Kt of either competitor changed substantially when compared with rats subjected to acute galactosemia. At 10 mM galactose in plasma in rats with acute galactosemia, the inhibition of glucose transport, simulated a 25% reduction of plasma glucose, and in rats with chronic galactosemia a 20% reduction. This moderate effect is in contrast to the effect of galactose in suckling rats in which 10 mM galactose in plasma reduced the glucose transport to a level corresponding to a 50% reduction of the plasma glucose concentration.",
author = "A Gjedde",
year = "1984",
language = "English",
volume = "43",
pages = "1654--62",
journal = "Journal of Neurochemistry",
issn = "0022-3042",
publisher = "Wiley-Blackwell",
number = "6",

}

RIS

TY - JOUR

T1 - Blood-brain transfer of galactose in experimental galactosemia, with special reference to the competitive interaction between galactose and glucose.

AU - Gjedde, A

PY - 1984

Y1 - 1984

N2 - The interaction between glucose and galactose during transport across the cerebral capillary endothelium was studied in anesthetized rats. Although galactose is present in the diet of suckling mammals and is a potential substrate for brain metabolism in adult mammals, its effect on glucose transport in adult rats is unknown. A kinetic model was formulated to analyze the effect of chronically elevated galactose levels on glucose transport in adult rats. The analysis indicated that galactose and glucose compete for the same transport mechanism in the cerebral capillary endothelium. The Tmax of glucose and galactose were both about 380 mumol 100 g-1 min-1 and the Kt of galactose (30 mM) was about three times that of glucose (10 mM). During prolonged galactosemia in adult rats, neither the Tmax, nor the Kt of either competitor changed substantially when compared with rats subjected to acute galactosemia. At 10 mM galactose in plasma in rats with acute galactosemia, the inhibition of glucose transport, simulated a 25% reduction of plasma glucose, and in rats with chronic galactosemia a 20% reduction. This moderate effect is in contrast to the effect of galactose in suckling rats in which 10 mM galactose in plasma reduced the glucose transport to a level corresponding to a 50% reduction of the plasma glucose concentration.

AB - The interaction between glucose and galactose during transport across the cerebral capillary endothelium was studied in anesthetized rats. Although galactose is present in the diet of suckling mammals and is a potential substrate for brain metabolism in adult mammals, its effect on glucose transport in adult rats is unknown. A kinetic model was formulated to analyze the effect of chronically elevated galactose levels on glucose transport in adult rats. The analysis indicated that galactose and glucose compete for the same transport mechanism in the cerebral capillary endothelium. The Tmax of glucose and galactose were both about 380 mumol 100 g-1 min-1 and the Kt of galactose (30 mM) was about three times that of glucose (10 mM). During prolonged galactosemia in adult rats, neither the Tmax, nor the Kt of either competitor changed substantially when compared with rats subjected to acute galactosemia. At 10 mM galactose in plasma in rats with acute galactosemia, the inhibition of glucose transport, simulated a 25% reduction of plasma glucose, and in rats with chronic galactosemia a 20% reduction. This moderate effect is in contrast to the effect of galactose in suckling rats in which 10 mM galactose in plasma reduced the glucose transport to a level corresponding to a 50% reduction of the plasma glucose concentration.

M3 - Journal article

C2 - 6491672

VL - 43

SP - 1654

EP - 1662

JO - Journal of Neurochemistry

JF - Journal of Neurochemistry

SN - 0022-3042

IS - 6

ER -

ID: 14946084