Bykov I, Järveläinen H, Lindros K
Department of Mental Health and Alcohol Research, National Public Health Institute, POB 33, 00251 Helsinki, Finland.
Alcohol Alcohol. 2003 Sep-Oct;38(5):400-6. doi: 10.1093/alcalc/agg109.
Excessive alcohol intake induces hepatic fatty infiltration, which has been suggested to sensitize the liver to further damage. To test this hypothesis, L-carnitine, a constitutional lipotropic compound, was administered to rats chronically treated with ethanol by liquid diet feeding for 10 weeks.
Ethanol administration caused marked steatosis, mild inflammation and elevated plasma alanine aminotransferase and tumour necrosis factor alpha (TNF-alpha) concentrations. Dietary supplementation with L-carnitine significantly reduced all these parameters as well as the hepatic concentration of thiobarbituric acid reactive substances, an indicator of lipid peroxidation products. Pretreatment with L-carnitine also significantly blunted ethanol-induced stimulation of TNF-alpha release by isolated Kupffer cells.
This study provides direct support for the notion that steatosis sensitizes the liver to further damage and suggests an involvement of TNF-alpha in this process.
过量饮酒会导致肝脏脂肪浸润,有人认为这会使肝脏对进一步损伤更加敏感。为了验证这一假设,将左旋肉碱(一种促脂化合物)给予通过液体饮食喂养10周长期接受乙醇处理的大鼠。
给予乙醇导致明显的脂肪变性、轻度炎症以及血浆丙氨酸转氨酶和肿瘤坏死因子α(TNF-α)浓度升高。补充左旋肉碱饮食可显著降低所有这些参数以及硫代巴比妥酸反应性物质的肝脏浓度,硫代巴比妥酸反应性物质是脂质过氧化产物的一个指标。左旋肉碱预处理还显著减弱了乙醇诱导的分离枯否细胞释放TNF-α的刺激。
本研究为脂肪变性使肝脏对进一步损伤更加敏感这一观点提供了直接支持,并表明TNF-α参与了这一过程。