Molecular mechanism of ER stress response by alcohol abuse.

为了阐明酒精滥用引起内质网应激反应的分子机制，我重点研究了在内质网附近观察到的脂质积累和脂代谢。肌酸是影响脂代谢的因素之一。由于新机构的搬迁，我不得不建立新的大鼠肝细胞原代培养实验室系统。我检查了新系统中的文化状况。进行大鼠肝细胞原代培养，在含0~10%血清的培养液中负载0~100 mM乙醇24小时。我发现乙醇抑制了血清肌酸的浓度，肌酸从肌酸转化而来，并随着培养液中血清浓度的增加而增加。肌酸是在肝脏中合成的，肌酸在脂质代谢中起着重要作用。酒精可抑制肝脏肌酸合成，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.