Ethanol (EtOH) consumption is a primary health risk worldwide, which generally starts during adolescence in a binge pattern (i.e., the episodic consumption of high amounts). Binge EtOH consumption can lead to modifications of the innate and adaptive immune responses, including fever. The present study evaluated the febrile response that was induced by lipopolysaccharide (LPS) and prostaglandins E2 (PGE2) and the mechanisms of thermoregulation in adolescent rats that were exposed to EtOH in a binge-like pattern. Male Wistar rats were treated with an intraperitoneal (i.p.) injection of EtOH or saline on postnatal days (PND) 25, 26, 29, 30, 33, 34, 37, and 38. On PND 51, they received a pyrogenic challenge with LPS (i.p.) or PGE2 (intracerebroventricular) to induce a febrile response. Interscapular brown adipose tissue (BAT) mass and uncoupling protein (UCP) activity in isolated mitochondria were evaluated on PND 51. The rats were then subjected to cold challenges to analyze adaptive thermogenesis. Intermittent EtOH exposure during adolescence impaired the LPS- and PGE2-induced febrile response 12 days after the end of EtOH exposure. Ethanol exposure decreased interscapular BAT mass, oxygen consumption, and UCP activity in isolated mitochondria, resulting in an impairment in thermogenesis at 5 °C. No morphological changes in BAT were observed. These findings indicate that binge-like EtOH exposure during adolescence impairs thermoregulation by reducing BAT mass and function. This reduction may last for a prolonged period of time after the cessation of EtOH exposure and may affect both cold defenses and the febrile response during the development of infectious diseases.

中文翻译：

---

青春期期间间歇性暴饮暴食性乙醇暴露通过减少大鼠棕色脂肪组织的生热作用而减弱了发热反应。

乙醇（EtOH）的消费是全球范围内的主要健康风险，通常在青春期以暴饮暴食的方式开始（即，大量的情节性消费）。大量摄入EtOH会导致先天性和适应性免疫反应的改变，包括发烧。本研究评估了脂多糖（LPS）和前列腺素E2（PGE2）诱导的发热反应，以及以暴饮暴食模式暴露于EtOH的青春期大鼠的体温调节机制。在出生后第25、26、29、30、33、34、37和38天，对Wistar雄性大鼠腹膜内（ip）注射EtOH或生理盐水。在PND 51上，他们接受LPS的热原性攻击（ip）或PGE2（脑室内）诱发发热反应。在PND 51上评估分离的线粒体中肩cap间棕色脂肪组织（BAT）的质量和解偶联蛋白（UCP）的活性。然后对大鼠进行冷刺激以分析适应性产热。青春期期间间歇性暴露于EtOH会在EtOH暴露结束12天后削弱LPS和PGE2诱导的发热反应。乙醇暴露降低了孤立线粒体的肩inter间BAT质量，耗氧量和UCP活性，导致在5°C下生热受损。没有观察到BAT的形态变化。这些发现表明，青春期暴饮暴食般的EtOH暴露会通过降低BAT的质量和功能而损害体温调节。