Analysis of hepatic genes involved in the metabolism of fatty acids and iron in nonalcoholic fatty liver disease

• Published in: Hepatology research 2009-04, Vol.39 (4), p.366-373
• Main Authors: Mitsuyoshi, Hironori, Yasui, Kohichiroh, Harano, Yuichi, Endo, Mio, Tsuji, Kazuhiro, Minami, Masahito, Itoh, Yoshito, Okanoue, Takeshi, Yoshikawa, Toshikazu
• Format: Article
• Language: English
• Subjects: fatty acids; iron; NAFLD; oxidative stress
• ISSN: 1386-6346; 1872-034X
• DOI: 10.1111/j.1872-034X.2008.00464.x

Aims:  Hepatic steatosis and iron cause oxidative stress, thereby progressing steatosis to steatohepatitis. We quantified the expression of genes involved in the metabolism of fatty acids and iron in patients with nonalcoholic fatty liver disease (NAFLD). Methods:  The levels of transcripts for the following genes were quantified from biopsy specimens of 74 patients with NAFLD: thioredoxin (Trx), fatty acid transport protein 5 (FATP5), sterol regulatory element‐binding protein 1c (SREBP1c), fatty acid synthase (FASN), acetyl‐coenzyme A carboxylase (ACAC), peroxisome proliferative activated receptor α (PPARα), cytochrome P‐450 2E1 (CYP2E1), acyl‐coenzyme A dehydrogenase (ACADM), acyl‐coenzyme A oxidase (ACOX), microsomal triglyceride transfer protein (MTP), transferrin receptor 1 (TfR1), transferrin receptor 2 (TfR2) and hepcidin. Twelve samples of human liver RNA were used as controls. Histological evaluation followed the methods of Brunt. Results:  The levels of all genes were significantly higher in the NAFLD patients than in controls. The Trx level increased as the stage progressed. The levels of FATP5, SREBP1c, ACAC, PPARα, CYP2E1, ACADM and MTP significantly decreased as the stage and grade progressed (P