Bradford Blair U, Rusyn Ivan
Department of Environmental Sciences and Engineering, School of Public Health, University of North Carolina, Chapel Hill, 27599-7431, USA.
Alcohol. 2005 Jan;35(1):13-7. doi: 10.1016/j.alcohol.2004.12.001.
The swift increase in alcohol metabolism (SIAM) is a phenomenon defined as a rapid increase in hepatic respiration and alcohol metabolism after administration of a bolus dose of alcohol. Continuous exposure to alcohol is known to produce adaptive changes in liver alcohol and oxygen metabolism. A considerable burst of hepatic respiration can also occur after administration of a single large dose of alcohol and results in a near doubling of alcohol metabolism, a high demand for oxygen, and downstream or pericentral hypoxia. These dramatic changes in rates of alcohol metabolism and tissue concentrations of oxygen are not due to induced enzyme activity in liver. This phenomenon depends on activation of mitochondrial function, an increase in co-factor supply for nicotinamide adenine dinucleotide-dependent alcohol metabolism, depletion of glycogen reserves, liberation of fatty acids through activation of an adrenergic response to alcohol providing substrate for catalase, and activation of Kupffer cells, the hepatic resident macrophages responsible for production of cytokines and prostaglandins. An understanding of the mechanisms of hypermetabolism in liver can have vital ramifications for knowledge of both alcohol-related and alcohol-unrelated liver injury because hypoxia that is a result of hypermetabolism can compound effects of pharmaceuticals and environmental agents on the liver. Swift increase in alcohol metabolism is an excellent example of the complexity of cell-cell interactions in liver and extrahepatic regulation of biochemical and molecular events in this organ, and this important phenomenon shall be considered in studies of liver disease and biochemistry.
酒精代谢快速增加（SIAM）是一种现象，定义为静脉注射一剂酒精后肝脏呼吸和酒精代谢的快速增加。已知持续接触酒精会在肝脏酒精和氧代谢中产生适应性变化。单次大剂量饮酒后也会出现相当程度的肝脏呼吸爆发，导致酒精代谢几乎翻倍、对氧气的高需求以及下游或中央周围缺氧。酒精代谢率和组织氧浓度的这些显著变化并非由于肝脏中诱导酶活性所致。这种现象取决于线粒体功能的激活、烟酰胺腺嘌呤二核苷酸依赖性酒精代谢的辅助因子供应增加、糖原储备的消耗、通过激活对酒精的肾上腺素能反应释放脂肪酸为过氧化氢酶提供底物，以及库普弗细胞的激活，库普弗细胞是肝脏驻留巨噬细胞，负责细胞因子和前列腺素的产生。了解肝脏高代谢机制对于认识酒精相关和非酒精相关肝损伤都可能产生至关重要的影响，因为高代谢导致的缺氧会加重药物和环境因素对肝脏的影响。酒精代谢快速增加是肝脏细胞间相互作用复杂性以及该器官生化和分子事件肝外调节的一个绝佳例子，在肝病和生物化学研究中应考虑这一重要现象。
