Masaki Kato

TL;DR: It is shown that mice with a targeted disruption of Lrp5 develop a low bone mass phenotype, and it is demonstrated that this phenotype becomes evident postnatally, and that it is secondary to decreased osteoblast proliferation and function in a Cbfa1-independent manner.

TL;DR: Examination of expression of fatty acid metabolism-related genes in NAFLD indicated increased de novo synthesis and uptake of fatty acids lead to further fatty acid accumulation in hepatocytes, and antioxidant pathways are activated to neutralize reactive oxygen species (ROS), which are overproduced during oxidative processes.

TL;DR: Analysis of the expression of genes regulating fatty acid synthesis by real-time PCR indicates that, in NAFLD, insulin signaling via IRS-1 causes the up-regulation of SREBP1-c, leading to the increased synthesis of fatty acids by the hepatocytes; negative feedback regulation via AMPK does not occur and the activation of Foxa2, following a decrease of IRS-2, up-regulates fatty acid oxidation.

TL;DR: This work investigated the transcriptional factors and lipogenic genes activated in the liver with NAFLD and found that SREBP‐1c and ChREBP are transactivated by liver X receptor (LXR), a nuclear receptor that regulates the metabolism of cholesterol and fatty acids.

TL;DR: Results indicate that both rho p21 and rho GDI, but neither rac p21 nor ras p21, are involved in the HGF-induced cell motility.