Transgenic expression of mutant peroxisome proliferator–activated receptor γ in liver precipitates fasting–induced steatosis but protects against high-fat diet–induced steatosis in mice
Steatosis is one of the most common liver diseases and is associated with the metabolic syndrome. A line of evidence suggests that peroxisome proliferator–activated receptor (PPAR) α and PPAR γ are involved in its pathogenesis. Hepatic overexpression of PPAR γ1 in mice provokes steatosis, whereas li...
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| Published in: | Metabolism, clinical and experimental Vol. 54; no. 11; pp. 1490 - 1498 |
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| Main Authors: | , , , , , , , , , , , , , , |
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| Abstract | Steatosis is one of the most common liver diseases and is associated with the metabolic syndrome. A line of evidence suggests that peroxisome proliferator–activated receptor (PPAR)
α and PPAR
γ are involved in its pathogenesis. Hepatic overexpression of PPAR
γ1 in mice provokes steatosis, whereas liver-specific PPAR
γ disruption ameliorates steatosis in
ob/ob mice, suggesting that hepatic PPAR
γ functions as an aggravator of steatosis. In contrast, PPAR
α-null mice are susceptible to steatosis because of reduced hepatic fatty acid oxidation. PPAR
γ with mutations in its C-terminal ligand-binding domain (L468A/E471A mutant PPAR
γ1) have been reported as a constitutive repressor of both PPAR
α and PPAR
γ activities in vitro. To elucidate the effect of cosuppression of PPAR
α and PPAR
γ on steatosis, we generated mutant PPAR
γ transgenic mice (Liver mt PPAR
γ Tg) under the control of liver-specific human serum amyloid P component promoter. In the liver of transgenic mice, PPAR
α and PPAR
γ agonist–induced augmentation of the expression of downstream target genes of PPAR
α and PPAR
γ, respectively, was significantly attenuated, suggesting PPAR
α and PPAR
γ cosuppression in vivo. Suppression of PPAR
α and PPAR
γ target genes was also observed in the fasted and high-fat–fed conditions. Liver mt PPAR
γ Tg were susceptible to fasting-induced steatosis while being protected against high-fat diet–induced steatosis. The opposite hepatic outcomes in Liver mt PPAR
γ Tg as a result of fasting and high-fat feeding may indicate distinct roles of PPAR
α and PPAR
γ in 2 different types of nutritionally provoked steatosis. |
|---|---|
| AbstractList | Steatosis is one of the most common liver diseases and is associated with the metabolic syndrome. A line of evidence suggests that peroxisome proliferator-activated receptor (PPAR) alpha and PPARgamma are involved in its pathogenesis. Hepatic overexpression of PPARgamma1 in mice provokes steatosis, whereas liver-specific PPARgamma disruption ameliorates steatosis in ob/ob mice, suggesting that hepatic PPARgamma functions as an aggravator of steatosis. In contrast, PPARalpha-null mice are susceptible to steatosis because of reduced hepatic fatty acid oxidation. PPARgamma with mutations in its C-terminal ligand-binding domain (L468A/E471A mutant PPARgamma1) have been reported as a constitutive repressor of both PPARalpha and PPARgamma activities in vitro. To elucidate the effect of co-suppression of PPARalpha and PPARgamma on steatosis, we generated mutant PPARgamma transgenic mice (Liver mt PPARgamma Tg) under the control of liver-specific human serum amyloid P component promoter. In the liver of transgenic mice, PPARalpha and PPARgamma agonist-induced augmentation of the expression of downstream target genes of PPARalpha and PPARgamma, respectively, was significantly attenuated, suggesting PPARalpha and PPARgamma co-suppression in vivo. Suppression of PPARalpha and PPARgamma target genes was also observed in the fasted and high-fat-fed conditions. Liver mt PPARgamma Tg were susceptible to fasting-induced steatosis while being protected against high-fat diet-induced steatosis. The opposite hepatic outcomes in Liver mt PPARgamma Tg as a result of fasting and high-fat feeding may indicate distinct roles of PPARalpha and PPARgamma in 2 different types of nutritionally provoked steatosis. Steatosis is one of the most common liver diseases and is associated with the metabolic syndrome. A line of evidence suggests that peroxisome proliferator–activated receptor (PPAR) α and PPAR γ are involved in its pathogenesis. Hepatic overexpression of PPAR γ1 in mice provokes steatosis, whereas liver-specific PPAR γ disruption ameliorates steatosis in ob/ob mice, suggesting that hepatic PPAR γ functions as an aggravator of steatosis. In contrast, PPAR α-null mice are susceptible to steatosis because of reduced hepatic fatty acid oxidation. PPAR γ with mutations in its C-terminal ligand-binding domain (L468A/E471A mutant PPAR γ1) have been reported as a constitutive repressor of both PPAR α and PPAR γ activities in vitro. To elucidate the effect of cosuppression of PPAR α and PPAR γ on steatosis, we generated mutant PPAR γ transgenic mice (Liver mt PPAR γ Tg) under the control of liver-specific human serum amyloid P component promoter. In the liver of transgenic mice, PPAR α and PPAR γ agonist–induced augmentation of the expression of downstream target genes of PPAR α and PPAR γ, respectively, was significantly attenuated, suggesting PPAR α and PPAR γ cosuppression in vivo. Suppression of PPAR α and PPAR γ target genes was also observed in the fasted and high-fat–fed conditions. Liver mt PPAR γ Tg were susceptible to fasting-induced steatosis while being protected against high-fat diet–induced steatosis. The opposite hepatic outcomes in Liver mt PPAR γ Tg as a result of fasting and high-fat feeding may indicate distinct roles of PPAR α and PPAR γ in 2 different types of nutritionally provoked steatosis. |
| Author | Masuzaki, Hiroaki Hayashi, Tatsuya Fujimoto, Muneya Ogawa, Yoshihiro Yukioka, Hideo Nakao, Kazuwa Tanaka, Tomohiro Hosoda, Kiminori Miyazawa, Takashi Yasue, Shintaro Miyanaga, Fumiko Ebihara, Ken Kobayashi, Nozomi Chusho, Hideki Kusakabe, Toru |
| Author_xml | – sequence: 1 givenname: Tomohiro surname: Tanaka fullname: Tanaka, Tomohiro organization: Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan – sequence: 2 givenname: Hiroaki surname: Masuzaki fullname: Masuzaki, Hiroaki email: hiroaki@kuhp.kyoto-u.ac.jp organization: Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan – sequence: 3 givenname: Ken surname: Ebihara fullname: Ebihara, Ken organization: Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan – sequence: 4 givenname: Yoshihiro surname: Ogawa fullname: Ogawa, Yoshihiro organization: Department of Molecular Medicine and Metabolism, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, 101-0062, Japan – sequence: 5 givenname: Shintaro surname: Yasue fullname: Yasue, Shintaro organization: Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan – sequence: 6 givenname: Hideo surname: Yukioka fullname: Yukioka, Hideo organization: Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan – sequence: 7 givenname: Hideki surname: Chusho fullname: Chusho, Hideki organization: Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan – sequence: 8 givenname: Fumiko surname: Miyanaga fullname: Miyanaga, Fumiko organization: Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan – sequence: 9 givenname: Takashi surname: Miyazawa fullname: Miyazawa, Takashi organization: Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan – sequence: 10 givenname: Muneya surname: Fujimoto fullname: Fujimoto, Muneya organization: Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan – sequence: 11 givenname: Toru surname: Kusakabe fullname: Kusakabe, Toru organization: Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan – sequence: 12 givenname: Nozomi surname: Kobayashi fullname: Kobayashi, Nozomi organization: Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan – sequence: 13 givenname: Tatsuya surname: Hayashi fullname: Hayashi, Tatsuya organization: Department of Human Coexistence, Kyoto University Graduate School of Human and Environmental Studies, Kyoto, 606-8501, Japan – sequence: 14 givenname: Kiminori surname: Hosoda fullname: Hosoda, Kiminori organization: Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan – sequence: 15 givenname: Kazuwa surname: Nakao fullname: Nakao, Kazuwa organization: Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/16253638$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Animals Dietary Fats - pharmacology Fasting Fatty Liver - etiology Fatty Liver - physiopathology Fatty Liver - prevention & control Gene Expression - physiology Genes, Dominant Humans Liver - physiology Male Mice Mice, Inbred C57BL Mice, Transgenic PPAR alpha - genetics PPAR alpha - metabolism PPAR gamma - genetics PPAR gamma - metabolism Promoter Regions, Genetic Recombinant Fusion Proteins - genetics Recombinant Fusion Proteins - metabolism RNA, Messenger - analysis Serum Amyloid P-Component - genetics Up-Regulation |
| Title | Transgenic expression of mutant peroxisome proliferator–activated receptor γ in liver precipitates fasting–induced steatosis but protects against high-fat diet–induced steatosis in mice |
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