ポスター発表
第2日 6月11日(火) P会場(多目的ホール・大会議室101+102)P1会場(多目的ホール)・P2会場(会議室101+102)
- 2P-27
肝線維化を呈する肝臓特異的67-kDa laminin receptor ノックアウトマウスのメタボローム解析
(九大院農)
o一瀬智美・ 米山拓良・ 竹下菜津子・ 錦戸里紗・ 熊添基文・ 藤村由紀・ 立花宏文
The 67-kDa laminin receptor (67LR) functions as a receptor for epigallocatechin-3-O-gallate (EGCG), a type of green tea catechin. However, the biological roles of 67LR are unclear. Liver-specific 67LR knockout (67LR-KO) mice showed liver fibrosis. In this study, we investigated the relationship between metabolic states and the progression of liver fibrosis in 67LR-KO mice by metabolomic analysis. Hydrophilic metabolites extracted from livers were analyzed using LC-MS-based targeted metabolomics. The LC-MS datasets were subjected to multivariate statistical analyses. The liver metabolome data from 67LR-KO and control mice were subjected to principal component analysis (PCA), which showed different variance between the two groups on the score plots, and also genotypic differences were observed in orthogonal partial least squares discriminant analysis (OPLS-DA). Metabolites reported to be decreased in mouse models of liver fibrosis tended to be decreased in 67LR-KO mice. The levels of some metabolites from various pathways were altered by 67LR-KO.
The presence of multiple metabolites in the liver of 67LR-KO mice, depending on their fibrotic status, these metabolic changes may be associated with liver fibrosis in 67LR-KO.