PPARa Expression Protects Male Mice from High Fat–Induced Nonalcoholic Fatty Liver  

Oleh:

Abdelmegeed, Mohamed A. ; Seong-Ho, Yoo ; Henderson, Lauren E. ; Gonzalez, Frank J. ; Woodcroft, Kimberley J. ; Byoung-Joon, Song

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: JN: The Journal of Nutrition vol. 141 no. 04 (Apr. 2011), page 603-610 .
Topik: FAT; Fatty Liver; High-Fat Diet

Ketersediaan

Perpustakaan FK Nomor Panggil: J42.K.2011.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

Lihat Detail Induk

Isi artikel

Emerging evidence suggests that the lack of PPARa enhances hepatic steatosis and inflammation in Ppara-null mice when fed a high-fat diet (HFD). Thus, the aim of this study was to determine whether Ppara-null mice are more susceptible to nonalcoholic steatohepatitis (NASH) than their wild-type (WT) counterparts following short-term feeding with a HFD. Age-matched male WT and Ppara-null mice were randomly assigned to consume ad libitum a standard Lieber-DeCarli liquid diet (STD) (35% energy from fat) or a HFD (71% energy from fat) for 3 wk. Liver histology, plasma transaminase levels, and indicators of oxidative/nitrosative stress and inflammatory cytokines were evaluated in all groups. Levels of lobular inflammation and the NASH activity score were greater in HFD-exposed Ppara-null mice than in the other 3 groups. Biochemical analysis revealed elevated levels of ethanol-inducible cytochrome P450 2E1 and TNFa accompanied by increased levels of malondialdehyde as well as oxidized and nitrated proteins in Ppara-null mice. Elevated oxidative stress and inflammation were associated with activation of c-Jun-N-terminal kinase and p38 kinase, resulting in increased hepatocyte apoptosis in Ppara-null mice fed a HFD. These results, with increased steatosis, oxidative stress, and inflammation observed in Ppara-null mice fed a HFD, demonstrate that inhibition of PPARa functions may increase susceptibility to high fat–induced NASH.

Opini Anda

Klik untuk menuliskan opini Anda tentang koleksi ini!

Kembali