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Brain energy consumption in ethanol-treated, Long-Evans rats
J R Viña1, J E Salus, M R DeJoseph
1Department of Physiology and Biophysics, University of Health Sciences, Chicago Medical School, Illinois 60064.
The Journal of Nutrition
|June 1, 1991
Summary
Chronic ethanol consumption alters brain glucose utilization. Acute intoxication significantly reduces cerebral metabolic rate of glucose utilization (CMRGlc), while chronic intake has a milder effect, with CMRGlc increasing after ethanol withdrawal.
Area of Science:
- Neuroscience
- Biochemistry
- Toxicology
Background:
- Ethanol consumption significantly impacts brain function.
- Understanding the effects of ethanol on cerebral metabolic rate of glucose utilization (CMRGlc) is crucial for assessing brain health.
- Previous studies have shown varied effects of ethanol on brain metabolism.
Purpose of the Study:
- To investigate the effects of chronic and acute ethanol administration on CMRGlc in rats.
- To examine the impact of ethanol withdrawal on brain glucose utilization.
- To correlate neuropathological findings with metabolic changes.
Main Methods:
- Rats were fed liquid diets containing ethanol for 8 weeks or received acute ethanol intoxication.
- Control rats were pair-fed isoenergetic diets with dextrin-maltose.
- Quantitative autogradiography with [6-14C]glucose and digital imaging techniques were used to measure CMRGlc in individual brain structures.
Main Results:
- Acute ethanol intoxication decreased CMRGlc across the brain, particularly in auditory, visual, memory, and motor areas.
- Chronic ethanol consumption had a less pronounced effect on CMRGlc compared to acute intoxication.
- After 18 hours of ethanol withdrawal, chronic ethanol-treated rats showed elevated CMRGlc levels above control values, without signs of seizures or dysfunction.
Conclusions:
- Acute ethanol intoxication significantly impairs brain glucose metabolism.
- Chronic ethanol consumption has a moderate impact on CMRGlc, with distinct regional effects.
- Ethanol withdrawal in chronically exposed rats leads to a compensatory increase in CMRGlc, indicating adaptive metabolic changes without overt neurological impairment.