Premium
Effects of Alcohol and Acetate on Cerebral Blood Flow: A Pilot Study
Author(s) -
Tanabe Jody,
Yamamoto Dorothy J.,
Sutton Brianne,
Brown Mark S.,
Hoffman Paula L.,
Burnham Ellen L.,
Glueck Deborah H.,
Tabakoff Boris
Publication year - 2019
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.14173
Subject(s) - placebo , cerebral blood flow , alcohol , medicine , anesthesia , ethanol , anterior cingulate cortex , nucleus accumbens , endocrinology , pharmacology , chemistry , receptor , biochemistry , pathology , psychiatry , alternative medicine , cognition
Background Acute alcohol produces effects on cerebral metabolism and blood flow. Alcohol is converted to acetate, which serves as a source of energy for the brain and is an agonist at G protein‐coupled receptors distributed in different cell types in the body including neurons. Acetate has been hypothesized to play a role in the cerebral blood flow (CBF) response after alcohol ingestion. We tested whether administration of acetate would alter CBF in a pattern similar to or different from that of alcohol ingestion in healthy individuals. Methods Twenty‐four healthy participants were assigned by convenience to receive either 0.6 g/kg alcohol orally ( n = 12) or acetate intravenously ( n = 12). For each participant, CBF maps were acquired using an arterial spin labeling sequence on a 3T magnetic resonance scanner after placebo and after drug administration. Whole‐brain CBF maps were compared between placebo and drug using a paired t ‐test, and set at a threshold of p < 0.05 corrected for multiple comparisons ( k ≥ 142 voxels, ≥3.78 cm 3 ), voxel‐level p < 0.005. Intoxication was measured after placebo and drug administration with a Subjective High Assessment Scale (SHAS‐7). Results Compared to placebo, alcohol and acetate were associated with increased CBF in the medial thalamus. Alcohol, but not acetate, was associated with increased CBF in the right orbitofrontal, medial prefrontal and cingulate cortex, and hippocampus. Plasma acetate levels increased following administration of alcohol and acetate and did not differ between the 2 arms. Alcohol, but not acetate, was associated with an increase in SHAS‐7 scores ( p < 0.001). Conclusions Increased thalamic CBF associated with either alcohol or acetate administration suggests that the thalamic CBF response after alcohol could be mediated by acetate. Compared to other brain regions, thalamus may differ in its ability to metabolize acetate or expression of receptors responsive to acetate. Increased prefrontal and limbic CBF associated with alcohol may be linked to alcohol's behavioral effects.