French S W
UCLA School of Medicine.
Alcohol Alcohol. 1993 Jan;28(1):97-109.
The data and experimental results reviewed here allow the construction of the following hypothesis: alcohol-induced liver disease results from a combination of two phenomena. The first is the induction of the maximum activity of CYP 2E1 by several dietary factors, i.e. (1) low carbohydrate-high fat diet; and (2) the dietary fats composed of PUFA (Yang et al., 1992). The second is the production of lipid peroxidation induced by CYP 2E1 oxidation of ethanol maintained at high blood alcohol levels (> 200 mg %) with the availability of PUFA as substrate (Ekstrom and Ingelman-Sundberg, 1988; Koop, 1992). Thus, lipid peroxidation may be the final common pathway which supports the induction of ALD. Further, it may provide the common denominator which links ALD pathogenesis to non-alcoholic steato-hepatitis (NASH) (French et al., 1989b), where CYP 2E1 is induced by high fat diet and/or diabetes (Dong et al., 1988).
酒精性肝病是由两种现象共同作用导致的。第一种现象是几种饮食因素诱导细胞色素P450 2E1（CYP 2E1）达到最大活性，即：（1）低碳水高脂肪饮食；（2）由多不饱和脂肪酸（PUFA）组成的膳食脂肪（Yang等人，1992年）。第二种现象是在高血醇水平（>200mg%）下，以PUFA为底物，由乙醇经CYP 2E1氧化诱导产生脂质过氧化（Ekstrom和Ingelman-Sundberg，1988年；Koop，1992年）。因此，脂质过氧化可能是支持酒精性肝病发生的最终共同途径。此外，它可能是将酒精性肝病发病机制与非酒精性脂肪性肝炎（NASH）联系起来的共同因素（French等人，1989b），在非酒精性脂肪性肝炎中，高脂肪饮食和/或糖尿病可诱导CYP 2E1产生（Dong等人，1988年）。
