Chronic alcohol consumption has emerged as a leading cause of metabolic derangement in susceptible cohorts worldwide; ethanol has a high calorific value and excessive intake interferes with energy metabolism. It has a very high glycemic index, so the glucose homeostasis does not follow the normal physiological regulations in chronic consumption of ethanol. Chronic alcohol consumption is a global concern for its health issues. The detailed mechanism of alcohol-associated organ damage and health anomalies has been reviewed here. Almost all of its metabolic fates has minor to major impacts on any physiological process. The main rate-limiting markers of glucose homeostasis, i.e. NADH/NAD+ and ATP/ADP, are physiologically misjudged in ethanol consumption; as a result, excess acetoacetyl CoA becomes engaged in ketone body formation resulting in ketoacidosis. Ethanol induced ROS production and antioxidant depletion resulting in necrotic tissue damage especially in the stomach, intestine epithelial cells, and liver. Increased oxidative stress causes vascular dysfunction, NO deregulation, peripheral vascular resistance, increased blood pressure, and aldosterone-induced hypertension. Ethanol manipulates intracellular phosphorylation regulations by influencing MAPK and inflammatory molecule, like TNFa and IL-6, and transcriptional stress factor like NF-κβ, Nrf-2, and Hif-α via redox signalling. Activation of lipogenic factors and PPAR signalling drastically increase body fat accumulation. Direct damage to the pancreatic cells generates insulin resistance. Synergistic effects of several metabolic malfunctioning develop insulin resistance, chronic hyperglycaemia, and abnormal fat accumulation.

中文翻译：

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长期饮酒的不良影响

慢性饮酒已成为全球易感人群代谢紊乱的主要原因；乙醇的发热量高，摄入过多会干扰能量代谢。它具有非常高的血糖指数，因此在长期饮用乙醇时，葡萄糖体内稳态不遵循正常的生理规律。长期饮酒对其健康问题是全球关注的问题。酒精相关器官损害和健康异常的详细机制已在这里进行了综述。它几乎所有的代谢命运对任何生理过程都具有次要的或重大的影响。葡萄糖稳态的主要限速标志物，即NADH / NAD +和ATP / ADP，在乙醇摄入中在生理上被误判。结果是，过量的乙酰乙酰基CoA参与酮体形成，导致酮症酸中毒。乙醇引起ROS的产生和抗氧化剂的消耗，特别是在胃，肠上皮细胞和肝脏中，导致坏死组织受损。氧化应激增加会导致血管功能障碍，NO失调，外周血管阻力，血压升高和醛固酮诱发的高血压。乙醇通过氧化还原信号通过影响MAPK和炎症分子（如TNFa和IL-6）和转录应激因子（如NF-κβ，Nrf-2和Hif-α）来操纵细胞内磷酸化调节。脂肪形成因子的激活和PPAR信号传导大大增加了体内脂肪的积累。对胰腺细胞的直接损害会产生胰岛素抵抗。