A group led by Associate Professor Hiroyuki Inuzuka of Tohoku University elucidated the mechanism of fatty liver onset caused by excessive intake of a high-fat diet.This is the result of joint research with the Beth Israel Deaconess Medical Center in the United States and Harvard Medical School.It is expected to contribute to the development of preventive and therapeutic methods for fatty liver disease.

 With the westernization of eating habits, non-alcoholic fatty liver disease (NAFLD) is increasing year by year, and it is considered to be the most frequent liver disease in developed countries.It is estimated that 1 to 3% of adults are affected in Japan as well.

 In cells, a proteolytic mechanism called the ubiquitin-proteasome system is involved in the regulation of cell functions such as cell cycle, immunity, and metabolism.Among them, beta-TRCP1 is said to regulate cell function by binding to various intracellular proteins and leading to degradation.

 This time, for the purpose of elucidating the function of beta-TRCP1, we searched for the substrate of beta-TRCP1 and identified a new substrate protein called Lipin1. Since Lipin1 has been reported to promote fat consumption in the liver and suppress fat synthesis, it is expected that beta-TRCP1 will promote fat synthesis in the liver by degrading the Lipin1 protein. Was done.

 Therefore, when beta-TRCP1 was deleted in cultured liver cells, the Lipin1 protein was not degraded but accumulated intracellularly, and the amount of fat synthesized in the cells decreased.Furthermore, beta-TRCP1 knockout mice and wild-type mice lacking beta-TRCP1 were fed a high-fat diet for a long period of time, and the amount of fat accumulated in the liver was observed.As a result, it was found that fatty liver was observed in wild-type mice and suppressed in beta-TRCP1 knockout mice.

 It is expected that this achievement will lead to the development of effective preventive and therapeutic methods for fatty liver diseases such as NAFLD.

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