AJP - Endo Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Endocrinol Metab 270: E746-E751, 1996;
0193-1849/96 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hasselbalch, S. G.
Right arrow Articles by Paulson, O. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hasselbalch, S. G.
Right arrow Articles by Paulson, O. B.

AJP - Endocrinology and Metabolism, Vol 270, Issue 5 E746-E751, Copyright © 1996 by American Physiological Society

ARTICLES

Changes in cerebral blood flow and carbohydrate metabolism during acute hyperketonemia

S. G. Hasselbalch, P. L. Madsen, L. P. Hageman, K. S. Olsen, N. Justesen, S. Holm and O. B. Paulson
Department of Neurology, Rigshospitalet, Copenhagen, Denmark.

During starvation, brain energy metabolism in humans changes toward oxidation of ketone bodies. To investigate if this shift is directly coupled to circulating blood concentrations of ketone bodies, we measured global cerebral blood flow (CBF) and global cerebral carbohydrate metabolism with the Kety-Schmidt technique before and during intravenous infusion with ketone bodies. During acute hyperketonemia (mean beta-hydroxybutyrate blood concentration 2.16 mM), cerebral uptake of ketones increased from 1.11 to 5.60 mumol.100 g-1.min-1, counterbalanced by an equivalent reduction of the cerebral glucose metabolism from 25.8 to 17.2 mumol.100 g-1.min-1, with the net result being an unchanged cerebral uptake of carbohydrates. In accordance with this, global cerebral oxygen metabolism was not significantly altered (144 vs. 135 mumol.100 g-1.min-1). The unchanged global cerebral metabolic activity was accompanied by a 39% increase in CBF from 51.0 to 70.9 ml.100 g-1.min-1. Regional analysis of the glucose metabolism by positron emission tomography-[18F]fluoro-2-deoxy-D-glucose indicated that mesencephalon does not oxidize ketone bodies to the same extent as the rest of the brain. It was concluded that the immediate oxidation of ketone bodies induced a decrease in cerebral glucose uptake in spite of an adequate glucose supply to the brain. Furthermore, acute hyperketonemia caused a resetting of the coupling between CBF and metabolism that could not be explained by alterations in arterial CO2 tension or pH.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
M. A. Puchowicz, K. Xu, X. Sun, A. Ivy, D. Emancipator, and J. C. LaManna
Diet-induced ketosis increases capillary density without altered blood flow in rat brain
Am J Physiol Endocrinol Metab, June 1, 2007; 292(6): E1607 - E1615.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
G. Blomqvist, M. Alvarsson, V. Grill, G. Von Heijne, M. Ingvar, J. O. Thorell, S. Stone-Elander, L. Widen, and K. Ekberg
Effect of acute hyperketonemia on the cerebral uptake of ketone bodies in nondiabetic subjects and IDDM patients
Am J Physiol Endocrinol Metab, July 1, 2002; 283(1): E20 - E28.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online