The fate of glucose during the period of decreased metabolism after fluid percussion injury: a 13C NMR study.

The present study determined the metabolic fate of [1, 2 13C2] glucose in male control rats and in rats with moderate lateral fluid percussion injured (FPI) at 3.5 h and 24 h post-surgery. After a 3-h infusion, the amount of 13C-labeled glucose increased bilaterally (26% in left/injured cerebral cortex and 45% in right cerebral cortex) at 3.

Glucose metabolism after traumatic brain injury: estimation of pyruvate carboxylase and pyruvate dehydrogenase flux by mass isotopomer analysis.

The metabolism of [1, 2 (13)C(2)] glucose via the tricarboxylic acid (TCA) cycle yields a number of key glutamate mass isotopomers whose formation is a function of pyruvate carboxylase (PC) and pyruvate dehydrogenase (PDH). Analysis of the isotopomer distribution patterns was used to determine the relative flux of glucose entry into the TCA cycle through anaplerotic and oxidative pathways in the cerebral cortex of both uninjured and traumatically injured adult male rats. In the cerebral cortex of uninjured animals the PC/PDH ratio showed greater metabolism of glucose via pyruvate carboxylase, which is consistent with the notion that the majority of glucose taken up at rest is used as a substrate for anaplerotic processes and not as an energy source.

Upregulation of pentose phosphate pathway and preservation of tricarboxylic acid cycle flux after experimental brain injury.

The metabolic fate of [1,2 13C]-labeled glucose was determined in male control and unilateral controlled cortical impact (CCI) injured rats at 3.5 and 24 h after surgery. The concentration of 13C-labeled glucose, lactate, glutamate and glutamine were measured in the injured and contralateral cortex.

Cell-permeant calcium buffer induced neuroprotection after cortical devascularization.

An excitotoxic cascade resulting in a significant intracellular calcium load is thought to be a primary mechanism leading to neuronal death after ischemia. One way to protect neurons from injury is through the use of cell-permeant calcium buffers. These molecules have been reported to be neuroprotective via their ability to increase the cell's overall Ca(2+) buffering load as well as by attenuating neurotransmitter release.

Cerebral glucose metabolism and the glutamine cycle as detected by in vivo and in vitro 13C NMR spectroscopy.

We review briefly 13C NMR studies of cerebral glucose metabolism with an emphasis on the roles of glial energetics and the glutamine cycle. Mathematical modeling analysis of in vivo 13C turnover experiments from the C4 carbons of glutamate and glutamine are consistent with: (i) the glutamine cycle being the major cerebral metabolic route supporting glutamatergic neurotransmission, (ii) glial glutamine synthesis being stoichiometrically coupled to glycolytic ATP production, (iii) glutamine serving as the main precursor of neurotransmitter glutamate and (iv) glutamatergic neurotransmission being supported by lactate oxidation in the neurons in a process accounting for 60-80% of the energy derived from glucose catabolism. However, more recent experimental approaches using inhibitors of the glial tricarboxylic acid (TCA) cycle (trifluoroacetic acid, TFA) or of glutamine synthase (methionine sulfoximine, MSO) reveal that a considerable portion of the energy required to support glutamine synthesis is derived from the oxidative metabolism of glucose in the astroglia and that a significant amount of the neurotransmitter glutamate is produced from neuronal glucose or lactate rather than from glial glutamine.