Leyva Leandro Ruiz, Salguero Agustín, Virgolini Miriam Beatriz, Romero Verónica Leonor, Marengo Leonardo, Fabio María Carolina, Morón Ignacio, Cendán Cruz Miguel, Pautassi Ricardo Marcos
Department of Pharmacology, Institute of Neuroscience, Biomedical Research Center (CIBM) Faculty of Medicine, University of Granada, and Instituto de Investigación Biosanitaria (ibs.GRANADA), Granada, Spain.
Instituto de Investigación Médica M. y M. Ferreyra (INIMEC - CONICET-Universidad Nacional de Córdoba), Córdoba 5000, Argentina.
Drug Alcohol Depend. 2023 Feb 1;243:109737. doi: 10.1016/j.drugalcdep.2022.109737. Epub 2022 Dec 9.
Ethanol drinking begins during adolescence and, particularly when occurs in a binge-like pattern, exerts lingering adverse consequences. Pre-clinical studies indicate that intermittent ethanol exposure (IEA, a model of repeated ethanol intoxication), or binge eating (BE) can increase subsequent ethanol consumption. It is unknown if the promoting effects of BE upon ethanol drinking are found in female rats and are modulated by IEA at adolescence. This study assessed interactive effects between IEA and BE, upon ethanol drinking.
Female Wistar rats were given 4.0 g/kg ethanol, every other day from postnatal day 25-45. At adulthood, they were exposed to sessions in which a brief offering of a sizeable portion of highly palatable sugary pills was followed by a 120-min exposure to an ethanol bottle.
Exploratory activity and recognition memory was not affected by the IEA. Glutathione peroxidase and catalase activity, and lipid peroxidation (measured in blood and brain at the end of the procedure) were not significantly affected by IEA or BE exposure. BE alone had a mild promoting effect on ethanol ingestion. Those rats that underwent IEA and BE, however, exhibited heightened and sustained ethanol self-administration (average of 2.12 g/kg/120 min, vs 1.15 g/kg/120 min of the other groups), that persisted throughout the BE sessions. IEA and a history of BE also promoted ethanol intake or preference in a two-bottle endpoint test.
The study suggests that exposure to IEA exerts, when followed by BE at adulthood, promoting effects upon ethanol intake, particularly at concentrations ≥ 6%.
饮酒始于青春期，尤其是以暴饮暴食的方式饮酒，会产生长期的不良后果。临床前研究表明，间歇性乙醇暴露（IEA，一种反复乙醇中毒的模型）或暴饮暴食（BE）会增加随后的乙醇摄入量。尚不清楚暴饮暴食对雌性大鼠乙醇摄入的促进作用是否存在，以及在青春期是否受间歇性乙醇暴露的调节。本研究评估了间歇性乙醇暴露和暴饮暴食对乙醇摄入的交互作用。
从出生后第25天至45天，每隔一天给雌性Wistar大鼠灌胃4.0 g/kg乙醇。成年后，让它们接触这样的实验环节：先短暂提供大量美味的含糖丸剂，然后让它们接触乙醇瓶120分钟。
间歇性乙醇暴露对探索活动和识别记忆没有影响。谷胱甘肽过氧化物酶和过氧化氢酶活性以及脂质过氧化（在实验结束时在血液和大脑中测量）不受间歇性乙醇暴露或暴饮暴食的显著影响。单独的暴饮暴食对乙醇摄入有轻微的促进作用。然而，那些经历了间歇性乙醇暴露和暴饮暴食的大鼠表现出更高且持续的乙醇自我给药量（平均为2.12 g/kg/120分钟，而其他组为1.15 g/kg/120分钟），并且在整个暴饮暴食实验环节中都持续存在。在双瓶终点测试中，间歇性乙醇暴露和暴饮暴食史也促进了乙醇摄入或偏好。
该研究表明，成年后经历间歇性乙醇暴露后再进行暴饮暴食，会对乙醇摄入产生促进作用，尤其是在浓度≥6%时。
