Molecular mechanism of ER stress response by alcohol abuse.

为了阐明酒精滥用对内质网应激反应的分子机制，我重点研究了内质网附近的脂质积累和脂质代谢。肌酸是影响脂质代谢的因素之一。我必须建立新的大鼠原代肝细胞培养的实验室系统，因为要转移到新的研究所。我检查了新系统的培养情况。我进行了大鼠肝细胞原代培养，在0-10%血清的培养基中加载0-100 mM乙醇，培养24小时。我发现乙醇抑制了血清肌酐的浓度，它由肌酸转化而来，并随着培养基中血清浓度的增加而增加。肌酸在肝脏中合成，在脂质代谢中起重要作用。酒精可能抑制肝脏肌酸合成，导致内质网应激反应紊乱和酒精性肝病。

To clarify the molecular mechanism of endoplasmic reticulum(ER) stress response by alcohol abuse, I focused on the lipid accumulation and lipid metabolism, both observed nearby ER. Creatine is one of factors concerning lipid metabolism. I had to establish new lab system for primary rat hepatocyte culture, because of moving on new institutes. I checked the condition of culture in the new system. I performed primary rat hepatocyte culture and loaded 0-100 mM ethanol in the culture medium with 0-10% serum for 24 hours. I found that ethanol suppressed serum concentration of creatinine, which converted from creatine and increased depending on the concentration of serum in the culture medium. Creatine is synthesized in the liver and creatine plays important role in lipid metabolism. Alcohol may suppress creatine synthesis in the liver leading disturbance of ER stress response and alcoholic liver disease.