Alcohol decreases baseline brain glucose metabolism more in heavy drinkers than controls but has no effect on stimulation-induced metabolic increases
Abstract
During alcohol intoxication the human brain increases metabolism of acetate and decreases metabolism of glucose as energy substrate. Here we hypothesized that chronic heavy drinking facilitates this energy substrate shift both for baseline and stimulation conditions. To test this hypothesis we compared the effects of alcohol intoxication (0.75g/kg alcohol versus placebo) on brain glucose metabolism during video-stimulation (VS) versus when given with no-stimulation (NS), in 25 heavy drinkers (HD) and 23 healthy controls each of whom underwent four PET-¹⁸FDG scans. We showed that resting whole-brain glucose metabolism (placebo-NS) was lower in HD than controls (13%, p=0.04); that alcohol (compared to placebo) decreased metabolism more in HD (20±13%) than controls (9±11%, p=0.005) and in proportion to daily alcohol consumption (r=0.36, p=0.01) but found that alcohol did not reduce the metabolic increases in visual cortex from VS in either group. Instead, VS reduced alcohol-induced decreases in whole-brain glucose metabolism (10±12%) compared to NS in both groups (15±13%, p=0.04), consistent with stimulation-related glucose metabolism enhancement. These findings corroborate our hypothesis that heavy alcohol consumption facilitates use of alternative energy substrates (i.e. acetate) for resting activity during intoxication, which might persist through early sobriety, but indicate that glucose is still favored as energy substratemore »
- Authors:
-
- National Inst. on Alcohol Abuse and Alcoholism, Bethesda, MD (United States)
- Brookhaven National Lab. (BNL), Upton, NY (United States)
- Stony Brook Medicine, Stony Brook, NY (United States)
- Publication Date:
- Research Org.:
- Brookhaven National Laboratory (BNL), Upton, NY (United States)
- Sponsoring Org.:
- USDOE Office of Science (SC), Biological and Environmental Research (BER)
- OSTI Identifier:
- 1184511
- Report Number(s):
- BNL-107888-2015-JA
Journal ID: ISSN 0270-6474; R&D Project: MO-085; KP1602010; TRN: US1500518
- Grant/Contract Number:
- SC00112704
- Resource Type:
- Accepted Manuscript
- Journal Name:
- Journal of Neuroscience
- Additional Journal Information:
- Journal Volume: 35; Journal Issue: 7; Journal ID: ISSN 0270-6474
- Publisher:
- Society for Neuroscience
- Country of Publication:
- United States
- Language:
- English
- Subject:
- 38 RADIATION CHEMISTRY, RADIOCHEMISTRY, AND NUCLEAR CHEMISTRY; positron emission tomography (PET) facility
Citation Formats
Volkow, Nora D., Fowler, Joanna S., Wang, Gene-Jack, Kojori, Eshan Shokri, Benveniste, Helene, and Tomasi, Dardo. Alcohol decreases baseline brain glucose metabolism more in heavy drinkers than controls but has no effect on stimulation-induced metabolic increases. United States: N. p., 2015.
Web. doi:10.1523/JNEUROSCI.4877-14.2015.
Volkow, Nora D., Fowler, Joanna S., Wang, Gene-Jack, Kojori, Eshan Shokri, Benveniste, Helene, & Tomasi, Dardo. Alcohol decreases baseline brain glucose metabolism more in heavy drinkers than controls but has no effect on stimulation-induced metabolic increases. United States. https://doi.org/10.1523/JNEUROSCI.4877-14.2015
Volkow, Nora D., Fowler, Joanna S., Wang, Gene-Jack, Kojori, Eshan Shokri, Benveniste, Helene, and Tomasi, Dardo. Wed .
"Alcohol decreases baseline brain glucose metabolism more in heavy drinkers than controls but has no effect on stimulation-induced metabolic increases". United States. https://doi.org/10.1523/JNEUROSCI.4877-14.2015. https://www.osti.gov/servlets/purl/1184511.
@article{osti_1184511,
title = {Alcohol decreases baseline brain glucose metabolism more in heavy drinkers than controls but has no effect on stimulation-induced metabolic increases},
author = {Volkow, Nora D. and Fowler, Joanna S. and Wang, Gene-Jack and Kojori, Eshan Shokri and Benveniste, Helene and Tomasi, Dardo},
abstractNote = {During alcohol intoxication the human brain increases metabolism of acetate and decreases metabolism of glucose as energy substrate. Here we hypothesized that chronic heavy drinking facilitates this energy substrate shift both for baseline and stimulation conditions. To test this hypothesis we compared the effects of alcohol intoxication (0.75g/kg alcohol versus placebo) on brain glucose metabolism during video-stimulation (VS) versus when given with no-stimulation (NS), in 25 heavy drinkers (HD) and 23 healthy controls each of whom underwent four PET-¹⁸FDG scans. We showed that resting whole-brain glucose metabolism (placebo-NS) was lower in HD than controls (13%, p=0.04); that alcohol (compared to placebo) decreased metabolism more in HD (20±13%) than controls (9±11%, p=0.005) and in proportion to daily alcohol consumption (r=0.36, p=0.01) but found that alcohol did not reduce the metabolic increases in visual cortex from VS in either group. Instead, VS reduced alcohol-induced decreases in whole-brain glucose metabolism (10±12%) compared to NS in both groups (15±13%, p=0.04), consistent with stimulation-related glucose metabolism enhancement. These findings corroborate our hypothesis that heavy alcohol consumption facilitates use of alternative energy substrates (i.e. acetate) for resting activity during intoxication, which might persist through early sobriety, but indicate that glucose is still favored as energy substrate during brain stimulation. Our findings are consistent with reduced reliance on glucose as the main energy substrate for resting brain metabolism during intoxication (presumably shifting to acetate or other ketones) and a priming of this shift in heavy drinkers, which might make them vulnerable to energy deficits during withdrawal.},
doi = {10.1523/JNEUROSCI.4877-14.2015},
journal = {Journal of Neuroscience},
number = 7,
volume = 35,
place = {United States},
year = {Wed Feb 18 00:00:00 EST 2015},
month = {Wed Feb 18 00:00:00 EST 2015}
}
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