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Histone Deacetylase Gene Expression Following Binge Alcohol Consumption in Rats and Humans
Author(s) -
LópezMoreno Jose Antonio,
Marcos Miguel,
CallejaConde Javier,
EcheverryAlzate Victor,
Bühler Kora M.,
CostaAlba Pilar,
Bernardo Edgar,
Laso FranciscoJavier,
Rodríguez de Fonseca Fernando,
Nadal Roser,
Viveros Maria Paz,
Maldonado Rafael,
Giné Elena
Publication year - 2015
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.12850
Subject(s) - binge drinking , alcohol , gene expression , histone deacetylase 2 , endocrinology , hdac1 , medicine , alcohol intoxication , histone deacetylase , alcohol abuse , alcohol and health , histone , alcohol consumption , gene , chemistry , biochemistry , poison control , psychiatry , injury prevention , environmental health
Background Alcohol binge drinking is one of the most common patterns of excessive alcohol use and recent data would suggest that histone deacetylases ( HDAC s ) gene expression profiling could be useful as a biomarker for psychiatric disorders. Methods This study aimed to characterize the gene expression patterns of Hdac 1–11 in samples of rat peripheral blood, liver, heart, prefrontal cortex, and amygdala following repeated binge alcohol consumption and to determine the parallelism of Hdac gene expression between rats and humans in peripheral blood. To accomplish this goal, we examined Hdac gene expression following 1, 4, or 8 alcohol binges (3 g/kg, orally) in the rat, in patients who were admitted to the hospital emergency department for acute alcohol intoxication, and in rats trained in daily operant alcohol self‐administration. Results We primarily found that acute alcohol binging reduced gene expression ( Hdac1–10 ) in the peripheral blood of alcohol‐naïve rats and that this effect was attenuated following repeated alcohol binges. There was also a reduction of Hdac gene expression in the liver ( Hdac2,4,5 ), whereas there was increased expression in the heart ( Hdac1,7,8 ) and amygdala ( Hdac1,2,5 ). Additionally, increased blood alcohol concentrations were measured in rat blood at 1 to 4 hours following repeated alcohol binging, and the only group that developed hepatic steotosis (fatty liver) were those animals exposed to 8 alcohol binge events. Finally, both binge consumption of alcohol in humans and daily operant alcohol self‐administration in rats increased Hdac gene expression in peripheral blood. Conclusions Our results suggest that increases in HDAC gene expression within the peripheral blood are associated with chronic alcohol consumption, whereas HDAC gene expression is reduced following initial exposure to alcohol.