Involvement of microsomal triglyceride transfer protein in nonalcoholic steatohepatitis in novel spontaneous mouse model
Background & Aims Nonalcoholic fatty liver disease (NAFLD) is currently recognized as a global health issue and encompasses a wide spectrum of entities, ranging from simple hepatic steatosis to nonalcoholic steatohepatitis (NASH). The lack of a spontaneous animal model of NASH, however, has hamp...
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Published in | Journal of hepatology Vol. 52; no. 6; pp. 903 - 912 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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Kidlington
Elsevier B.V
01.06.2010
Elsevier |
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Abstract | Background & Aims Nonalcoholic fatty liver disease (NAFLD) is currently recognized as a global health issue and encompasses a wide spectrum of entities, ranging from simple hepatic steatosis to nonalcoholic steatohepatitis (NASH). The lack of a spontaneous animal model of NASH, however, has hampered basic research in this field. Methods We examined the hepatic lesions in the inbred Fatty Liver Shionogi (FLS) mouse, which exhibits type 2 diabetes, and investigated the molecular mechanism leading to NAFLD/NASH. Using vector-mediated hepatic expression of microsomal triglyceride transfer protein (MTP), a key molecule for very low density lipoprotein (VLDL) assembly and export, its contribution to the hepatic lesions as well as to glucose intolerance was examined. Results The FLS mouse, maintained on normal chow, exhibited excessive hepatic triglyceride (TG) accumulation due to impaired VLDL secretion, and subsequently hepatic lesions comparable to NASH, with increased expression of inflammatory molecules as well as insulin resistance. Gene expression and Western blot analyses demonstrated reduced hepatic expression of MTP in the FLS mouse. Hepatic induction of MTP resulted in a reduction in hepatic TG accumulation, improvement of VLDL export, and amelioration of NASH-like lesions, as well as glucose intolerance. Conclusions These data suggest that the FLS mouse could serve as a spontaneous model of NASH with insulin resistance, and that reduced MTP is involved in the development of NASH, pointing towards MTP as a critical target for the prevention and treatment of NASH. |
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AbstractList | BACKGROUND & AIMSNonalcoholic fatty liver disease (NAFLD) is currently recognized as a global health issue and encompasses a wide spectrum of entities, ranging from simple hepatic steatosis to nonalcoholic steatohepatitis (NASH). The lack of a spontaneous animal model of NASH, however, has hampered basic research in this field.METHODSWe examined the hepatic lesions in the inbred Fatty Liver Shionogi (FLS) mouse, which exhibits type 2 diabetes, and investigated the molecular mechanism leading to NAFLD/NASH. Using vector-mediated hepatic expression of microsomal triglyceride transfer protein (MTP), a key molecule for very low density lipoprotein (VLDL) assembly and export, its contribution to the hepatic lesions as well as to glucose intolerance was examined.RESULTSThe FLS mouse, maintained on normal chow, exhibited excessive hepatic triglyceride (TG) accumulation due to impaired VLDL secretion, and subsequently hepatic lesions comparable to NASH, with increased expression of inflammatory molecules as well as insulin resistance. Gene expression and Western blot analyses demonstrated reduced hepatic expression of MTP in the FLS mouse. Hepatic induction of MTP resulted in a reduction in hepatic TG accumulation, improvement of VLDL export, and amelioration of NASH-like lesions, as well as glucose intolerance.CONCLUSIONSThese data suggest that the FLS mouse could serve as a spontaneous model of NASH with insulin resistance, and that reduced MTP is involved in the development of NASH, pointing towards MTP as a critical target for the prevention and treatment of NASH. Background & Aims Nonalcoholic fatty liver disease (NAFLD) is currently recognized as a global health issue and encompasses a wide spectrum of entities, ranging from simple hepatic steatosis to nonalcoholic steatohepatitis (NASH). The lack of a spontaneous animal model of NASH, however, has hampered basic research in this field. Methods We examined the hepatic lesions in the inbred Fatty Liver Shionogi (FLS) mouse, which exhibits type 2 diabetes, and investigated the molecular mechanism leading to NAFLD/NASH. Using vector-mediated hepatic expression of microsomal triglyceride transfer protein (MTP), a key molecule for very low density lipoprotein (VLDL) assembly and export, its contribution to the hepatic lesions as well as to glucose intolerance was examined. Results The FLS mouse, maintained on normal chow, exhibited excessive hepatic triglyceride (TG) accumulation due to impaired VLDL secretion, and subsequently hepatic lesions comparable to NASH, with increased expression of inflammatory molecules as well as insulin resistance. Gene expression and Western blot analyses demonstrated reduced hepatic expression of MTP in the FLS mouse. Hepatic induction of MTP resulted in a reduction in hepatic TG accumulation, improvement of VLDL export, and amelioration of NASH-like lesions, as well as glucose intolerance. Conclusions These data suggest that the FLS mouse could serve as a spontaneous model of NASH with insulin resistance, and that reduced MTP is involved in the development of NASH, pointing towards MTP as a critical target for the prevention and treatment of NASH. Nonalcoholic fatty liver disease (NAFLD) is currently recognized as a global health issue and encompasses a wide spectrum of entities, ranging from simple hepatic steatosis to nonalcoholic steatohepatitis (NASH). The lack of a spontaneous animal model of NASH, however, has hampered basic research in this field. We examined the hepatic lesions in the inbred Fatty Liver Shionogi (FLS) mouse, which exhibits type 2 diabetes, and investigated the molecular mechanism leading to NAFLD/NASH. Using vector-mediated hepatic expression of microsomal triglyceride transfer protein (MTP), a key molecule for very low density lipoprotein (VLDL) assembly and export, its contribution to the hepatic lesions as well as to glucose intolerance was examined. The FLS mouse, maintained on normal chow, exhibited excessive hepatic triglyceride (TG) accumulation due to impaired VLDL secretion, and subsequently hepatic lesions comparable to NASH, with increased expression of inflammatory molecules as well as insulin resistance. Gene expression and Western blot analyses demonstrated reduced hepatic expression of MTP in the FLS mouse. Hepatic induction of MTP resulted in a reduction in hepatic TG accumulation, improvement of VLDL export, and amelioration of NASH-like lesions, as well as glucose intolerance. These data suggest that the FLS mouse could serve as a spontaneous model of NASH with insulin resistance, and that reduced MTP is involved in the development of NASH, pointing towards MTP as a critical target for the prevention and treatment of NASH. |
Author | Rakugi, Hiromi Wang, Xiang Sugimoto, Ken Shindo, Nobuyasu Fujisawa, Tomomi Nojima, Koji Yasuda, Osamu Ikegami, Hiroshi Yoshikawa, Yuki Oze-Fukai, Aya |
Author_xml | – sequence: 1 fullname: Shindo, Nobuyasu – sequence: 2 fullname: Fujisawa, Tomomi – sequence: 3 fullname: Sugimoto, Ken – sequence: 4 fullname: Nojima, Koji – sequence: 5 fullname: Oze-Fukai, Aya – sequence: 6 fullname: Yoshikawa, Yuki – sequence: 7 fullname: Wang, Xiang – sequence: 8 fullname: Yasuda, Osamu – sequence: 9 fullname: Ikegami, Hiroshi – sequence: 10 fullname: Rakugi, Hiromi |
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Copyright | European Association for the Study of the Liver 2010 European Association for the Study of the Liver 2015 INIST-CNRS Copyright 2010 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved. |
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Keywords | triglyceride NAFLD MCP-1 Spontaneous model Glucose intolerance Irs1 MTP alanine aminotransferase monocyte chemoattractant protein-1 microsomal triglyceride transfer protein ALT Irs2 F4/80 nonalcoholic steatohepatitis B6 mouse FLS mouse Fatty Liver Shionogi mouse VLDL gamma-glutamyltransferase ApoB HPLC cell surface glycoprotein F4/80 BMI AST body mass index homeostasis model assessment ratio NASH aspartate aminotransferase C57BL/6 mouse intraperitoneal glucose tolerance test nonalcoholic fatty liver disease high performance liquid chromatography insulin receptor substrate 2 TG insulin receptor substrate 1 TNF-α GGT tumor necrosis factor-α Insulin resistance very low density lipoprotein HOMA-R ipGTT apolipoprotein B Nonalcoholic steatohepatitis Microsomal triglyceride transfer protein Endocrinopathy Spontaneous Rodentia Metabolic diseases Triglyceride Protein Target tissue resistance Vertebrata Mammalia Mouse Animal Gastroenterology Models Impaired glucose tolerance |
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Snippet | Background & Aims Nonalcoholic fatty liver disease (NAFLD) is currently recognized as a global health issue and encompasses a wide spectrum of entities,... Nonalcoholic fatty liver disease (NAFLD) is currently recognized as a global health issue and encompasses a wide spectrum of entities, ranging from simple... BACKGROUND & AIMSNonalcoholic fatty liver disease (NAFLD) is currently recognized as a global health issue and encompasses a wide spectrum of entities, ranging... |
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SubjectTerms | Animals Biological and medical sciences Blood Glucose - metabolism Carrier Proteins - genetics Carrier Proteins - metabolism Cholesterol, VLDL - blood Diabetes. Impaired glucose tolerance Disease Models, Animal Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Fatty Liver - metabolism Fatty Liver - pathology Fatty Liver - physiopathology Gastroenterology and Hepatology Gastroenterology. Liver. Pancreas. Abdomen Gene Expression - physiology Glucose intolerance Glucose Intolerance - metabolism Glucose Intolerance - pathology Glucose Intolerance - physiopathology Insulin - blood Insulin resistance Insulin Resistance - physiology Lipid Metabolism - genetics Liver - metabolism Liver - pathology Liver Cirrhosis - metabolism Liver Cirrhosis - pathology Liver Cirrhosis - physiopathology Male Medical sciences Mice Mice, Inbred C57BL Mice, Mutant Strains Microsomal triglyceride transfer protein Microsomes, Liver - metabolism Microsomes, Liver - pathology Nonalcoholic steatohepatitis Phenotype Spontaneous model Transfection Triglycerides - metabolism |
Title | Involvement of microsomal triglyceride transfer protein in nonalcoholic steatohepatitis in novel spontaneous mouse model |
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