Evaluation of fatty acid metabolism-related gene expression in nonalcoholic fatty liver disease

  • Authors:
    • Makoto Nakamuta
    • Motoyuki Kohjima
    • Shusuke Morizono
    • Kazuhiro Kotoh
    • Tsuyoshi Yoshimoto
    • Izuru Miyagi
    • Munechika Enjoji
  • View Affiliations

  • Published online on: October 1, 2005     https://doi.org/10.3892/ijmm.16.4.631
  • Pages: 631-635
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Abstract

Nonalcoholic fatty liver disease (NAFLD) is one of the most frequent causes of abnormal liver dysfunction, and its prevalence has markedly increased; however, the mechanisms involved in the pathogenesis of NAFLD have not been thoroughly investigated in humans. In this study, we evaluated the expression of fatty acid metabolism-related genes in NAFLD. Real-time RT-PCR was performed using liver biopsy samples from 12 NAFLD patients. The target genes studied were: acetyl-CoA carboxylase (ACC) 1, ACC2, and fatty acid synthase (FAS) for the evaluation of de novo fatty acid synthesis; carnitine palmitoyltransferase 1a (CPT1a), long-chain acyl-CoA dehydrogenase (LCAD), and long-chain L-3-hydroxyacyl-coenzyme A dehydrogenase α (HADHα) for β-oxidation in the mitochondria; peroxisome proliferator-activated receptor- (PPAR-) α and cytochrome P450 2E1 (CYP2E1) for oxidation in peroxisomes and microsomes (endoplasmic reticulum) respectively; and diacylglycerol O-acyltransferase 1 (DGAT1), PPAR-γ, and hormone sensitive lipase (HSL) for triglyceride synthesis and catalysis. In NAFLD, expression of ACC1 and ACC2, but not FAS was increased, indicating that de novo fatty acid synthesis is enhanced in NAFLD. In contrast, expression of CTP1a, a rate-limiting enzyme, was remarkably decreased, indicating that β-oxidation in the mitochondria was decreased, although the expression of LCAD and HADHα was increased. Expression of PPAR-α was increased, whereas that of CYP2E1 was reduced. The expression of DGAT1, PPAR-γ, and HSL was enhanced. These data suggest that in NAFLD, increased de novo synthesis and decreased β-oxidation in the mitochondria lead to accumulation of fatty acids in hepatocytes, although the extent of oxidation in peroxisomes and microsomes remains unclear.

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October 2005
Volume 16 Issue 4

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Nakamuta M, Kohjima M, Morizono S, Kotoh K, Yoshimoto T, Miyagi I and Enjoji M: Evaluation of fatty acid metabolism-related gene expression in nonalcoholic fatty liver disease. Int J Mol Med 16: 631-635, 2005.
APA
Nakamuta, M., Kohjima, M., Morizono, S., Kotoh, K., Yoshimoto, T., Miyagi, I., & Enjoji, M. (2005). Evaluation of fatty acid metabolism-related gene expression in nonalcoholic fatty liver disease. International Journal of Molecular Medicine, 16, 631-635. https://doi.org/10.3892/ijmm.16.4.631
MLA
Nakamuta, M., Kohjima, M., Morizono, S., Kotoh, K., Yoshimoto, T., Miyagi, I., Enjoji, M."Evaluation of fatty acid metabolism-related gene expression in nonalcoholic fatty liver disease". International Journal of Molecular Medicine 16.4 (2005): 631-635.
Chicago
Nakamuta, M., Kohjima, M., Morizono, S., Kotoh, K., Yoshimoto, T., Miyagi, I., Enjoji, M."Evaluation of fatty acid metabolism-related gene expression in nonalcoholic fatty liver disease". International Journal of Molecular Medicine 16, no. 4 (2005): 631-635. https://doi.org/10.3892/ijmm.16.4.631