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Local cerebral glucose consumption during insulin‐induced hypoglycemia, and in the recovery period following glucose administration

Local cerebral glucose consumption during insulin‐induced hypoglycemia, and in the recovery... Using the 14C‐deoxyglucose technique, we estimated local glucose consumption in the rat brain (1–CMRgl) in hypoglycemia of sufficient severity to cause cessation of spontaneous EEG activity, and in the recovery period following a 30 min period of such hypoglycemia. After 5 and 30 min of hypoglycemia, 1–CMRgl was markedly reduced in many cerebral structures (cerebral cortices, caudateputamen, thalamus, and hippocampus) but unchanged or only moderately reduced in other structures (cerebellar cortex, hypo thalamus, and pontine grey). The results indicate that differences in 1–CMRgl were caused by regional differences in the true or apparent kinetic constants for glucose transport, or that the consequences of a hypoglycemic derangement of cellular metabolism interfered with glucose transport in some regions. Local CMRgl was markedly heterogenous in the recovery period, induced by glucose administration in animals with a prior (30 min) period of hypoglycemia. In general, a reduced posthypoglycemic glucose consumption was correlated to low 1–CMRgl values during hypoglycemia. However, the hippocampus provided an exception since its CMRgl returned to control values. A correlation with previous measurement of local cerebral blood flow (1–CBF) demonstrates that regions having a pronounced reduction in 1–CMRgl during hypoglycemia developed a mismatch between blood flow and metabolic rate in the recovery period, the flow showing a disproportional reduction. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Acta Physiologica Wiley

Local cerebral glucose consumption during insulin‐induced hypoglycemia, and in the recovery period following glucose administration

ABDUL‐RAHMAN, A.; SIESJÖ, B. K.
Acta Physiologica , Volume 110 (2) – Oct 1, 1980
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References (21)

Publisher
Wiley
Copyright
Copyright © 1980 Wiley Subscription Services, Inc., A Wiley Company
ISSN
1748-1708
eISSN
1748-1716
DOI
10.1111/j.1748-1716.1980.tb06645.x
pmid
7010919
Publisher site
See Article on Publisher Site

Abstract

Using the 14C‐deoxyglucose technique, we estimated local glucose consumption in the rat brain (1–CMRgl) in hypoglycemia of sufficient severity to cause cessation of spontaneous EEG activity, and in the recovery period following a 30 min period of such hypoglycemia. After 5 and 30 min of hypoglycemia, 1–CMRgl was markedly reduced in many cerebral structures (cerebral cortices, caudateputamen, thalamus, and hippocampus) but unchanged or only moderately reduced in other structures (cerebellar cortex, hypo thalamus, and pontine grey). The results indicate that differences in 1–CMRgl were caused by regional differences in the true or apparent kinetic constants for glucose transport, or that the consequences of a hypoglycemic derangement of cellular metabolism interfered with glucose transport in some regions. Local CMRgl was markedly heterogenous in the recovery period, induced by glucose administration in animals with a prior (30 min) period of hypoglycemia. In general, a reduced posthypoglycemic glucose consumption was correlated to low 1–CMRgl values during hypoglycemia. However, the hippocampus provided an exception since its CMRgl returned to control values. A correlation with previous measurement of local cerebral blood flow (1–CBF) demonstrates that regions having a pronounced reduction in 1–CMRgl during hypoglycemia developed a mismatch between blood flow and metabolic rate in the recovery period, the flow showing a disproportional reduction.

Journal

Acta Physiologica – Wiley

Published: Oct 1, 1980

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