Effect of ethanol on glucose and amino acid metabolism in brain

Roach, Mary K.; Reese, W.N.

doi:10.1016/0006-2952(71)90191-2

Cited by 38 publications

(18 citation statements)

References 12 publications

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“…The 13 C enrichments of Glu 4 and Gln 4 for cortex and subcortex obtained after 2 hr of infusion are shown in Fig. 4 A and B.…”

Section: Resultsmentioning

confidence: 99%

“…Fig. 4 C and D shows the 13 C enrichments from Ac 12 , Ac 2 , and Etoh 2 in the cortex and subcortex regions, based on the isotopomers observed for Glu 4 and Gln 4 . Gln Etoh2 was significantly greater (P = 0.003) after Etoh chronic treated in cortex, and although Gln Ac2 was also higher, the treatment effect did not reach significance (P = 0.8).…”

Section: Resultsmentioning

confidence: 99%

“…Isotopomer Enrichment Patterns of Brain Glu 4 and Gln 4 . As a result of spin-spin splitting between the C3 and C4 carbons and the C4 and C5 carbons, it was feasible to differentiate metabolism of Ac 12 , which labels Gln and Glu always at both C4 and C5, from that of Ac 2 , which never labels Gln and Glu at C5.…”

Section: Resultsmentioning

confidence: 99%

“…Total Enrichments of Brain Glu 4 and Gln 4 . The 13 C enrichments of Glu 4 and Gln 4 for cortex and subcortex obtained after 2 hr of infusion are shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Acetate (Ac) generated from Etoh by the liver is consumed by the brain (3,4), where it replaces a significant portion of cerebral glucose metabolism in humans and animals (5)(6)(7)(8), either decreasing glucose consumption directly or compensating for glucose consumption decreased by some other effect. However, the brain may also oxidize Etoh (9)(10)(11)(12)(13)(14), and that capacity is important with respect to several perspectives.…”

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confidence: 99%

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Oxidation of ethanol in the rat brain and effects associated with chronic ethanol exposure

Wang

Jiang³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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It has been reported that chronic and acute alcohol exposure decreases cerebral glucose metabolism and increases acetate oxidation. However, it remains unknown how much ethanol the living brain can oxidize directly and whether such a process would be affected by alcohol exposure. The questions have implications for reward, oxidative damage, and long-term adaptation to drinking. One group of adult male Sprague-Dawley rats was treated with ethanol vapor and the other given room air. After 3 wk the rats received i.v. [2-13 C]ethanol and [1, 2-13 C 2 ]acetate for 2 h, and then the brain was fixed, removed, and divided into neocortex and subcortical tissues for measurement of 13 C isotopic labeling of glutamate and glutamine by magnetic resonance spectroscopy. Ethanol oxidation was seen to occur both in the cortex and the subcortex. In ethanol-naïve rats, cortical oxidation of ethanol occurred at rates of 0.017 ± 0.002 μmol/min/g in astroglia and 0.014 ± 0.003 μmol/min/g in neurons, and chronic alcohol exposure increased the astroglial ethanol oxidation to 0.028 ± 0.002 μmol/min/g (P = 0.001) with an insignificant effect on neuronal ethanol oxidation. Compared with published rates of overall oxidative metabolism in astroglia and neurons, ethanol provided 12.3 ± 1.4% of cortical astroglial oxidation in ethanol-naïve rats and 20.2 ± 1.5% in ethanol-treated rats. For cortical astroglia and neurons combined, the ethanol oxidation for naïve and treated rats was 3.2 ± 0.3% and 3.8 ± 0.2% of total oxidation, respectively. 13C labeling from subcortical oxidation of ethanol was similar to that seen in cortex but was not affected by chronic ethanol exposure.T he liver is the major organ for the oxidation of ethanol (Etoh) (1, 2), followed by the stomach and other organs. Acetate (Ac) generated from Etoh by the liver is consumed by the brain (3, 4), where it replaces a significant portion of cerebral glucose metabolism in humans and animals (5-8), either decreasing glucose consumption directly or compensating for glucose consumption decreased by some other effect. However, the brain may also oxidize Etoh (9-14), and that capacity is important with respect to several perspectives. The first step of Etoh oxidation generates acetaldehyde (AA), which is toxic, reactive, and potentially carcinogenic. AA is aversive systemically, as has been observed from the unpleasant effects of disulfuram, an inhibitor of AA dehydrogenase, but it has been shown to be rewarding in parts of the brain (12,15,16) especially in the posterior ventral tegmental area (17-19) by activating dopamine neurons (20)(21)(22). The liver maintains circulating levels of AA at levels of 20-155 μM (23, 24), and AA has been reported not to penetrate the blood-brain barrier or to penetrate very slowly (23,25). Thus, if the brain can oxidize Etoh, then intracerebral AA may mediate behavioral, neurochemical, and toxic effects of Etoh in the brain, possibly playing a role in the development of alcohol dependence (6,16,26).AA is difficult to measure in living systems. The ...

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“…The 13 C enrichments of Glu 4 and Gln 4 for cortex and subcortex obtained after 2 hr of infusion are shown in Fig. 4 A and B.…”

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

“…Total Enrichments of Brain Glu 4 and Gln 4 . The 13 C enrichments of Glu 4 and Gln 4 for cortex and subcortex obtained after 2 hr of infusion are shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

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Oxidation of ethanol in the rat brain and effects associated with chronic ethanol exposure

Wang

Jiang³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Ethanol during weaning induces a transient susceptibility to audiogenic seizures in Rb mice

Schreiber

Lehmann

1981

Developmental Psychobiology

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Metabolic changes in the rat brain after acute and chronic ethanol intoxication: A ³¹P NMR spectroscopy study

Denays

Chao

Mathur-De-Vré

et al. 1993

Magnetic Resonance in Med

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In this work, 31P phosphorus NMR (31P NMR) studies of the brain have been conducted in rats acutely and chronically intoxicated with ethanol. In both groups, changes in levels of high-energy phosphates were observed: increase of phosphocreatinine (PCr)/beta AaTP and PCr/inorganic phosphate (Pi) in acute and long-term ethanol exposure, and decrease of Pi/beta ATP after acute ethanol administration. These changes in high-energy phosphates, indicative of a reduction of adenosine triphosphate (ATP) and PCr consumption (PCr+ ADP+ H+ ATP+ Cr; ATP ADP+ Pi), suggest a reduction of cerebral metabolism both in acute and chronic ethanol exposure. In addition, in the group of rats chronically intoxicated with ethanol, there were variations in phosphodiester peak intensities (decrease of phosphomonoester (PME)/phosphodiester (PDE), increase of PDE/beta ATP), suggesting increased breakdown of membrane phospholipids. These changes could provide a metabolic explanation for the development of cerebral atrophy in chronic alcoholism.

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Effect of ethanol on glucose and amino acid metabolism in brain

Cited by 38 publications

References 12 publications

Oxidation of ethanol in the rat brain and effects associated with chronic ethanol exposure

Oxidation of ethanol in the rat brain and effects associated with chronic ethanol exposure

Ethanol during weaning induces a transient susceptibility to audiogenic seizures in Rb mice

Metabolic changes in the rat brain after acute and chronic ethanol intoxication: A ³¹P NMR spectroscopy study

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Effect of ethanol on glucose and amino acid metabolism in brain

Cited by 38 publications

References 12 publications

Oxidation of ethanol in the rat brain and effects associated with chronic ethanol exposure

Oxidation of ethanol in the rat brain and effects associated with chronic ethanol exposure

Ethanol during weaning induces a transient susceptibility to audiogenic seizures in Rb mice

Metabolic changes in the rat brain after acute and chronic ethanol intoxication: A 31P NMR spectroscopy study

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Metabolic changes in the rat brain after acute and chronic ethanol intoxication: A ³¹P NMR spectroscopy study