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1 potentially carcinogenic metabolites such as secondary bile acids.
2 nsistent with accumulation of TLCA and other secondary bile acids.
3 echanism underlying the oncogenic effects of secondary bile acids.
4 ficant shift in the abundance of primary and secondary bile acids.
5 lationship between polyp reduction and fecal secondary bile acids after feeding UDCA to these rats.
6 ected microbially modified molecules such as secondary bile acids and unexpected microbial molecules
7 rial 7 alpha-dehydroxylase and PI-PLC, fecal secondary bile acids, and colonic mucosal DAG kinase and
8 accompanied by decreased free and conjugated secondary bile acids as well as changes in gut microbiot
10 of dietary fat on colonic bacterial enzymes, secondary bile acids, colonic mucosal and tumor DAG kina
12 novel role for specific bile acids, and the secondary bile acid DCA in particular, in the regulation
14 enzyme also activates chenodeoxycholate, the secondary bile acids deoxycholate and lithocholate, and
23 carcinogenesis may include the production of secondary bile acids in the colon and the modulation of
24 Subsequently, mice were treated with these secondary bile acids in vivo to assess their ability to
25 t flora modify primary bile acids to produce secondary bile acids leading to a chemically diverse bil
27 hat VDR also functions as a receptor for the secondary bile acid lithocholic acid (LCA), which is hep
28 and lower fibre consumption, higher colonic secondary bile acids, lower colonic short-chain fatty ac
32 dehydroxylase that is involved in generating secondary bile acids, phosphatidylinositol-specific phos
34 rial and colonic mucosal enzymes and colonic secondary bile acids relevant to colon tumor promotion.
35 or) protects the body from hepatotoxicity of secondary bile acids such as lithocholic acid (LCA) by i
36 fed the HFCO diet excreted higher levels of secondary bile acids, such as deoxycholic acid and litho
37 rmentation and butyrogenesis, and suppressed secondary bile acid synthesis in the African Americans.
38 r M-BAR) is a G protein-coupled receptor for secondary bile acids that is highly expressed in monocyt
39 erol is converted into dozens of primary and secondary bile acids through pathways subject to negativ
40 human livers were incubated with primary and secondary bile acids to determine their effects on LCFA
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