Genetic analysis of expression profile involved in retinoid metabolism in non-alcoholic fatty liver disease

An Afida Ashla, Yoshiko Hoshikawa, Hiroyuki Tsuchiya, Koich Hashiguchi, Munechika Enjoji, Makoto Nakamuta, Akinobu Taketomi, Yoshihiko Maehara, Kohei Shomori, Akihiro Kurimasa, Ichiro Hisatome, Hisao Ito, Goshi Shiota

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Abstract

Aim: The patients with non-alcoholic fatty liver disease (NAFLD) have been reported to be at greater risk for progression to chronic liver disease including liver cirrhosis (LC). To examine the mechanisms for the progression of NAFLD, a genetic analysis of hepatic expression profile in retinoid metabolism in NAFLD was performed since the loss of retinoid signaling is associated with the progression of liver disease via reactive oxygen species (ROS) generation. Methods: Fifty-one genes, which are associated with retinoid metabolism and action, were examined in thirty six subjects including 17 patients with simple steatosis, 11 with non-alcoholic steatohepatitis (NASH) and eight controls were examined by real-time reverse transcriptase polymerase chain reaction. Immunohistochemical study was also done by 3 kinds of antibodies. Results: Higher expression of CRBP1 LRAT, DGT1/2 and CES1 in NAFLD suggests that mutual conversion between retinyl ester and retinal occurs actively. Expression of ADH1/2/3, RDH5/10/11, DHRS3 and RALDH1/3 was increased in NAFLD, suggesting that oxidation process from retinol to all-trans retinoic acid (ATRA) was enhanced. Importantly, greater expression of CYP26A1 indicated that degradation of ATRA was enhanced in NAFLD. Further, expression of SOD1/2, catalase, thioredoxin and uncoupling protein 2 was also enhanced. Conclusion: Hyperdynamic state of retinoid metabolism is present in the liver tissues with NAFLD, which may be a putative mechanism by which NAFLD progresses to chronic liver disease including LC.

Original languageEnglish
Pages (from-to)594-604
Number of pages11
JournalHepatology Research
Volume40
Issue number6
DOIs
Publication statusPublished - Jun 1 2010

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Retinoids
Liver Diseases
Tretinoin
Liver Cirrhosis
Chronic Disease
Thioredoxins
Non-alcoholic Fatty Liver Disease
Liver
Fatty Liver
Reverse Transcriptase Polymerase Chain Reaction
Vitamin A
Catalase
Real-Time Polymerase Chain Reaction
Reactive Oxygen Species
Esters
Antibodies
Genes

All Science Journal Classification (ASJC) codes

  • Hepatology
  • Infectious Diseases

Cite this

Ashla, A. A., Hoshikawa, Y., Tsuchiya, H., Hashiguchi, K., Enjoji, M., Nakamuta, M., ... Shiota, G. (2010). Genetic analysis of expression profile involved in retinoid metabolism in non-alcoholic fatty liver disease. Hepatology Research, 40(6), 594-604. https://doi.org/10.1111/j.1872-034X.2010.00646.x

Genetic analysis of expression profile involved in retinoid metabolism in non-alcoholic fatty liver disease. / Ashla, An Afida; Hoshikawa, Yoshiko; Tsuchiya, Hiroyuki; Hashiguchi, Koich; Enjoji, Munechika; Nakamuta, Makoto; Taketomi, Akinobu; Maehara, Yoshihiko; Shomori, Kohei; Kurimasa, Akihiro; Hisatome, Ichiro; Ito, Hisao; Shiota, Goshi.

In: Hepatology Research, Vol. 40, No. 6, 01.06.2010, p. 594-604.

Research output: Contribution to journalArticle

Ashla, AA, Hoshikawa, Y, Tsuchiya, H, Hashiguchi, K, Enjoji, M, Nakamuta, M, Taketomi, A, Maehara, Y, Shomori, K, Kurimasa, A, Hisatome, I, Ito, H & Shiota, G 2010, 'Genetic analysis of expression profile involved in retinoid metabolism in non-alcoholic fatty liver disease', Hepatology Research, vol. 40, no. 6, pp. 594-604. https://doi.org/10.1111/j.1872-034X.2010.00646.x
Ashla, An Afida ; Hoshikawa, Yoshiko ; Tsuchiya, Hiroyuki ; Hashiguchi, Koich ; Enjoji, Munechika ; Nakamuta, Makoto ; Taketomi, Akinobu ; Maehara, Yoshihiko ; Shomori, Kohei ; Kurimasa, Akihiro ; Hisatome, Ichiro ; Ito, Hisao ; Shiota, Goshi. / Genetic analysis of expression profile involved in retinoid metabolism in non-alcoholic fatty liver disease. In: Hepatology Research. 2010 ; Vol. 40, No. 6. pp. 594-604.
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AU - Ashla, An Afida

AU - Hoshikawa, Yoshiko

AU - Tsuchiya, Hiroyuki

AU - Hashiguchi, Koich

AU - Enjoji, Munechika

AU - Nakamuta, Makoto

AU - Taketomi, Akinobu

AU - Maehara, Yoshihiko

AU - Shomori, Kohei

AU - Kurimasa, Akihiro

AU - Hisatome, Ichiro

AU - Ito, Hisao

AU - Shiota, Goshi

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N2 - Aim: The patients with non-alcoholic fatty liver disease (NAFLD) have been reported to be at greater risk for progression to chronic liver disease including liver cirrhosis (LC). To examine the mechanisms for the progression of NAFLD, a genetic analysis of hepatic expression profile in retinoid metabolism in NAFLD was performed since the loss of retinoid signaling is associated with the progression of liver disease via reactive oxygen species (ROS) generation. Methods: Fifty-one genes, which are associated with retinoid metabolism and action, were examined in thirty six subjects including 17 patients with simple steatosis, 11 with non-alcoholic steatohepatitis (NASH) and eight controls were examined by real-time reverse transcriptase polymerase chain reaction. Immunohistochemical study was also done by 3 kinds of antibodies. Results: Higher expression of CRBP1 LRAT, DGT1/2 and CES1 in NAFLD suggests that mutual conversion between retinyl ester and retinal occurs actively. Expression of ADH1/2/3, RDH5/10/11, DHRS3 and RALDH1/3 was increased in NAFLD, suggesting that oxidation process from retinol to all-trans retinoic acid (ATRA) was enhanced. Importantly, greater expression of CYP26A1 indicated that degradation of ATRA was enhanced in NAFLD. Further, expression of SOD1/2, catalase, thioredoxin and uncoupling protein 2 was also enhanced. Conclusion: Hyperdynamic state of retinoid metabolism is present in the liver tissues with NAFLD, which may be a putative mechanism by which NAFLD progresses to chronic liver disease including LC.

AB - Aim: The patients with non-alcoholic fatty liver disease (NAFLD) have been reported to be at greater risk for progression to chronic liver disease including liver cirrhosis (LC). To examine the mechanisms for the progression of NAFLD, a genetic analysis of hepatic expression profile in retinoid metabolism in NAFLD was performed since the loss of retinoid signaling is associated with the progression of liver disease via reactive oxygen species (ROS) generation. Methods: Fifty-one genes, which are associated with retinoid metabolism and action, were examined in thirty six subjects including 17 patients with simple steatosis, 11 with non-alcoholic steatohepatitis (NASH) and eight controls were examined by real-time reverse transcriptase polymerase chain reaction. Immunohistochemical study was also done by 3 kinds of antibodies. Results: Higher expression of CRBP1 LRAT, DGT1/2 and CES1 in NAFLD suggests that mutual conversion between retinyl ester and retinal occurs actively. Expression of ADH1/2/3, RDH5/10/11, DHRS3 and RALDH1/3 was increased in NAFLD, suggesting that oxidation process from retinol to all-trans retinoic acid (ATRA) was enhanced. Importantly, greater expression of CYP26A1 indicated that degradation of ATRA was enhanced in NAFLD. Further, expression of SOD1/2, catalase, thioredoxin and uncoupling protein 2 was also enhanced. Conclusion: Hyperdynamic state of retinoid metabolism is present in the liver tissues with NAFLD, which may be a putative mechanism by which NAFLD progresses to chronic liver disease including LC.

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