Binge drinking is a remarkably prevalent behavior. In 2015, 27% of U.S. residents 18 years old or older reported at least one episode of binge drinking in the previous month. Rodent models for binge drinking are widely used to study the mechanisms by which alcohol causes a variety of adverse health effects in humans. Concerns have been raised that many binge-drinking studies in rodents involve alcohol doses that would be unrealistically high in humans. Allometric dosage scaling can be used to estimate the dose of a drug or chemical in mice that would be necessary to achieve similar biological effects at a realistic dose in humans. However, it has become apparent that no single allometric conversion factor is applicable for all drugs and chemicals, so it is necessary to evaluate each compound empirically. In the present study, we compared the area under the blood alcohol concentration vs. time curve (AUC) and the peak blood alcohol concentration following oral alcohol administration at various doses in mice and humans, using data from previously published studies. The results demonstrated that the oral dose of alcohol must be larger in mice (on a g of alcohol to kg of body weight basis) than in humans to achieve similar alcohol AUC values or to achieve similar peak concentrations in the blood. The dose required in mice was about 2-fold greater than the dose required in humans to achieve similar alcohol AUC and peak concentrations. The results shown here were substantially different from the average 5–12-fold difference between mice and humans calculated in previous studies using agents other than alcohol. Results shown here demonstrate that an empirical approach using data from several independent experiments provides information needed to determine the alcohol dose in mice that produces a similar level of exposure (AUC and peak concentration) as in humans. The results indicate that a single alcohol dose in the range of 5–6 g/kg, a range often used in mouse models for binge drinking, is not excessive when modeling human binge drinking. Results presented here illustrate that in mice both alcohol AUC and peak alcohol concentration correlate well with an important biological effect – activation of the hypothalamic-pituitary-adrenal axis – as indicated by increased corticosterone AUC values.

暴饮暴食是一种非常普遍的行为。2015 年，18 岁或以上的美国居民中有 27% 报告在上个月至少有一次暴饮暴食。用于狂饮的啮齿动物模型被广泛用于研究酒精对人类造成各种不利健康影响的机制。人们担心，许多啮齿动物酗酒研究涉及的酒精剂量在人类中会高得不切实际。异速生长剂量标度可用于估计药物或化学品在小鼠中的剂量，这对于在人类实际剂量下实现类似的生物效应是必要的。然而，很明显，没有单一的异速生长转换因子适用于所有药物和化学品，因此有必要凭经验评估每种化合物。在目前的研究中，我们使用先前发表的研究数据，比较了小鼠和人类口服不同剂量酒精后的血液酒精浓度与时间曲线 (AUC) 下的面积和血液酒精浓度峰值。结果表明，小鼠的酒精口服剂量（以酒精的重量比公斤体重计算）必须大于人类，以达到相似的酒精 AUC 值或达到相似的血液峰值浓度。小鼠所需的剂量比人类达到相似的酒精 AUC 和峰值浓度所需的剂量大约 2 倍。此处显示的结果与之前使用酒精以外的药物计算的小鼠和人类之间平均 5-12 倍的差异有很大不同。此处显示的结果表明，使用来自多个独立实验的数据的经验方法提供了确定小鼠酒精剂量所需的信息，该剂量产生与人类相似的暴露水平（AUC 和峰值浓度）。结果表明，5–6 g/kg 范围内的单一酒精剂量（该范围常用于小鼠模型中用于暴饮暴食）在模拟人类暴饮暴食时并不过分。此处显示的结果表明，在小鼠中，酒精 AUC 和峰值酒精浓度与重要的生物效应（下丘脑-垂体-肾上腺轴的激活）密切相关，如皮质酮 AUC 值增加所示。