ELSEVIER Neuroscience Research 26 (1996) 369-376
NEUROSCIENCE
RESEARCH
Lactate spares glucose as a metabolic fuel in neurons and astrocytes
from primary culture
A. Tabernero, C. Vicario, J.M. Medina*
Departamento de Bioquimica y Biologla Molecular, Edificio Departamental, Facultad de Farmacia, Universidad de Salamanca,
Ada Campo Charro s /n., E-37080 Salamanca, Spain
Received 25 July 1996; accepted 7 October 1996
Abstract
The effect of lactate on glucose metabolism in neurons and astrocytes from primary culture has been studied. The rates of
glucose metabolism through the pentose-phosphate shunt, the pyruvate dehydrogenase-catalyzed reaction, the tricarboxylic acid
cycle, the total lipogenesis and the synthesis of glycerol-borne lipids in astrocytes were 2-3 fold higher than in neurons. However,
the rate of glucose incorporation into sterols and esterified fatty acids was similar in both types of cells. Total glucose utilization
was inhibited by lactate to the same extend in both neurons and astrocytes. Lactate strongly inhibited glucose oxidation through
the pyruvate dehydrogenase-catalyzed reaction and the tricarboxylic acid cycle, in both neurons (60 and 44%, respectively) and
astrocytes (64 and 62%, respectively). Glucose incorporation into sterols and fatty acids was also inhibited by lactate in both
neurons and astrocytes (57 and 76%, respectively) while the oxidation of glucose in the pentose-phosphate shunt and the synthesis
of glycerol-borne lipids was not significantly affected. These results suggest that in the presence of lactate both neurons and
astrocytes can utilize lactate as the major metabolic substrate, sparing glucose for the synthesis of NADPH(H +), ribose-5-phos-
phate and/or glycerol-borne lipids. An interaction between glucose and lactate metabolism at the level of the pyruvate
dehydrogenase-catalyzed reaction is suggested. Copyright © 1996 Elsevier Science Ireland Ltd
Keywords: Brain; Metabolism; Hypoglycaemia; Hyperlactiacidemia
1. Introduction
Immediately after delivery, the rate of liver
glycogenolysis is very low (Cuezva et al., 1980; Fernan-
dez et al., 1983; Girard et al., 1973) and the gluconeo-
genic capacity of the liver is negligible (Fernandez et al.,
1983; Medina et al., 1980), resulting in very low plasma
concentrations of glucose (Cuezva et al., 1980; Girard
et al., 1973). However, lactate accumulates in the blood
during late gestation, reaching concentrations higher
than 9 mM during the first minutes of extrauterine life
Abbreviations: PBS, phosphate-buffered saline; BSA, fatty acid-free
bovine serum albumin; DMEM, Dulbecco's modified Eagle's
medium; FCS, fetal calf serum; EBS, Earle's balanced solution;
GFAP, glial fibrillary acidic protein.
*Corresponding author. Fax: +34 23 294564; e-mail: med-
ina@gugu.usal.es
(Cuezva et al., 1980; Juanes et al., 1986). In addition a
number of observations are consistent with the hypoth-
esis that lactate is an important metabolic substrate for
the brain during the early neonatal period (for a review
see, Medina et al., 1992). Moreover, some evidence
suggests that lactate plays a role in the traffic of
metabolites between neurons and astrocytes
(Magistretti et al., 1993; Poitry Yamate et al., 1995;
Sonnewald et al., 1995). In this context, glycogen, the
major brain energy reserve, is located mainly in astro-
cytes (Cataldo and Broadwell, 1986) but is responsible
for neuronal survival under glucose deprivation (Swan-
son and Choi, 1993). However, glycogen is released by
astrocytes as lactate (Dringen et al., 1993a) which is
presumably used by neurons as a source of energy and
carbon skeletons (Tabernero et al., 1993; Vicario et al.,
1993). In addition, lactate may be piped through astro-
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