Human translatability of the GAN diet-induced obese mouse model of non-alcoholic steatohepatitis

Abstract Background Animal models of non-alcoholic steatohepatitis (NASH) are important tools in preclinical research and drug discovery. Gubra-Amylin NASH (GAN) diet-induced obese (DIO) mice represent a model of fibrosing NASH. The present study directly assessed the clinical translatability of the...
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Autor*in:	Henrik H. Hansen [verfasserIn] Helene M. Ægidius [verfasserIn] Denise Oró [verfasserIn] Simon S. Evers [verfasserIn] Sara Heebøll [verfasserIn] Peter Lykke Eriksen [verfasserIn] Karen Louise Thomsen [verfasserIn] Anja Bengtsson [verfasserIn] Sanne S. Veidal [verfasserIn] Michel Feigh [verfasserIn] Malte P. Suppli [verfasserIn] Filip K. Knop [verfasserIn] Henning Grønbæk [verfasserIn] Diego Miranda [verfasserIn] James L. Trevaskis [verfasserIn] Niels Vrang [verfasserIn] Jacob Jelsing [verfasserIn] Kristoffer T. G. Rigbolt [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	Non-alcoholic steatohepatitis Mouse model Diet-induced obesity Translatability Histopathology Histomorphometry

Übergeordnetes Werk:	In: BMC Gastroenterology - BMC, 2003, 20(2020), 1, Seite 12
Übergeordnetes Werk:	volume:20 ; year:2020 ; number:1 ; pages:12

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/s12876-020-01356-2

Katalog-ID:	DOAJ043501761

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520			\|a Abstract Background Animal models of non-alcoholic steatohepatitis (NASH) are important tools in preclinical research and drug discovery. Gubra-Amylin NASH (GAN) diet-induced obese (DIO) mice represent a model of fibrosing NASH. The present study directly assessed the clinical translatability of the model by head-to-head comparison of liver biopsy histological and transcriptome changes in GAN DIO-NASH mouse and human NASH patients. Methods C57Bl/6 J mice were fed chow or the GAN diet rich in saturated fat (40%), fructose (22%) and cholesterol (2%) for ≥38 weeks. Metabolic parameters as well as plasma and liver biomarkers were assessed. Liver biopsy histology and transcriptome signatures were compared to samples from human lean individuals and patients diagnosed with NASH. Results Liver lesions in GAN DIO-NASH mice showed similar morphological characteristics compared to the NASH patient validation set, including macrosteatosis, lobular inflammation, hepatocyte ballooning degeneration and periportal/perisinusoidal fibrosis. Histomorphometric analysis indicated comparable increases in markers of hepatic lipid accumulation, inflammation and collagen deposition in GAN DIO-NASH mice and NASH patient samples. Liver biopsies from GAN DIO-NASH mice and NASH patients showed comparable dynamics in several gene expression pathways involved in NASH pathogenesis. Consistent with the clinical features of NASH, GAN DIO-NASH mice demonstrated key components of the metabolic syndrome, including obesity and impaired glucose tolerance. Conclusions The GAN DIO-NASH mouse model demonstrates good clinical translatability with respect to the histopathological, transcriptional and metabolic aspects of the human disease, highlighting the suitability of the GAN DIO-NASH mouse model for identifying therapeutic targets and characterizing novel drug therapies for NASH.
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650		4	\|a Diet-induced obesity
650		4	\|a Translatability
650		4	\|a Histopathology
650		4	\|a Histomorphometry
653		0	\|a Diseases of the digestive system. Gastroenterology
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700	0		\|a Niels Vrang \|e verfasserin \|4 aut
700	0		\|a Jacob Jelsing \|e verfasserin \|4 aut
700	0		\|a Kristoffer T. G. Rigbolt \|e verfasserin \|4 aut
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allfields	10.1186/s12876-020-01356-2 doi (DE-627)DOAJ043501761 (DE-599)DOAJ738511df0fdc4d36be87fd7875e0fda9 DE-627 ger DE-627 rakwb eng RC799-869 Henrik H. Hansen verfasserin aut Human translatability of the GAN diet-induced obese mouse model of non-alcoholic steatohepatitis 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Animal models of non-alcoholic steatohepatitis (NASH) are important tools in preclinical research and drug discovery. Gubra-Amylin NASH (GAN) diet-induced obese (DIO) mice represent a model of fibrosing NASH. The present study directly assessed the clinical translatability of the model by head-to-head comparison of liver biopsy histological and transcriptome changes in GAN DIO-NASH mouse and human NASH patients. Methods C57Bl/6 J mice were fed chow or the GAN diet rich in saturated fat (40%), fructose (22%) and cholesterol (2%) for ≥38 weeks. Metabolic parameters as well as plasma and liver biomarkers were assessed. Liver biopsy histology and transcriptome signatures were compared to samples from human lean individuals and patients diagnosed with NASH. Results Liver lesions in GAN DIO-NASH mice showed similar morphological characteristics compared to the NASH patient validation set, including macrosteatosis, lobular inflammation, hepatocyte ballooning degeneration and periportal/perisinusoidal fibrosis. Histomorphometric analysis indicated comparable increases in markers of hepatic lipid accumulation, inflammation and collagen deposition in GAN DIO-NASH mice and NASH patient samples. Liver biopsies from GAN DIO-NASH mice and NASH patients showed comparable dynamics in several gene expression pathways involved in NASH pathogenesis. Consistent with the clinical features of NASH, GAN DIO-NASH mice demonstrated key components of the metabolic syndrome, including obesity and impaired glucose tolerance. Conclusions The GAN DIO-NASH mouse model demonstrates good clinical translatability with respect to the histopathological, transcriptional and metabolic aspects of the human disease, highlighting the suitability of the GAN DIO-NASH mouse model for identifying therapeutic targets and characterizing novel drug therapies for NASH. Non-alcoholic steatohepatitis Mouse model Diet-induced obesity Translatability Histopathology Histomorphometry Diseases of the digestive system. Gastroenterology Helene M. Ægidius verfasserin aut Denise Oró verfasserin aut Simon S. Evers verfasserin aut Sara Heebøll verfasserin aut Peter Lykke Eriksen verfasserin aut Karen Louise Thomsen verfasserin aut Anja Bengtsson verfasserin aut Sanne S. Veidal verfasserin aut Michel Feigh verfasserin aut Malte P. Suppli verfasserin aut Filip K. Knop verfasserin aut Henning Grønbæk verfasserin aut Diego Miranda verfasserin aut James L. Trevaskis verfasserin aut Niels Vrang verfasserin aut Jacob Jelsing verfasserin aut Kristoffer T. G. Rigbolt verfasserin aut In BMC Gastroenterology BMC, 2003 20(2020), 1, Seite 12 (DE-627)326643702 (DE-600)2041351-8 1471230X nnns volume:20 year:2020 number:1 pages:12 https://doi.org/10.1186/s12876-020-01356-2 kostenfrei https://doaj.org/article/738511df0fdc4d36be87fd7875e0fda9 kostenfrei http://link.springer.com/article/10.1186/s12876-020-01356-2 kostenfrei https://doaj.org/toc/1471-230X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 20 2020 1 12
spelling	10.1186/s12876-020-01356-2 doi (DE-627)DOAJ043501761 (DE-599)DOAJ738511df0fdc4d36be87fd7875e0fda9 DE-627 ger DE-627 rakwb eng RC799-869 Henrik H. Hansen verfasserin aut Human translatability of the GAN diet-induced obese mouse model of non-alcoholic steatohepatitis 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Animal models of non-alcoholic steatohepatitis (NASH) are important tools in preclinical research and drug discovery. Gubra-Amylin NASH (GAN) diet-induced obese (DIO) mice represent a model of fibrosing NASH. The present study directly assessed the clinical translatability of the model by head-to-head comparison of liver biopsy histological and transcriptome changes in GAN DIO-NASH mouse and human NASH patients. Methods C57Bl/6 J mice were fed chow or the GAN diet rich in saturated fat (40%), fructose (22%) and cholesterol (2%) for ≥38 weeks. Metabolic parameters as well as plasma and liver biomarkers were assessed. Liver biopsy histology and transcriptome signatures were compared to samples from human lean individuals and patients diagnosed with NASH. Results Liver lesions in GAN DIO-NASH mice showed similar morphological characteristics compared to the NASH patient validation set, including macrosteatosis, lobular inflammation, hepatocyte ballooning degeneration and periportal/perisinusoidal fibrosis. Histomorphometric analysis indicated comparable increases in markers of hepatic lipid accumulation, inflammation and collagen deposition in GAN DIO-NASH mice and NASH patient samples. Liver biopsies from GAN DIO-NASH mice and NASH patients showed comparable dynamics in several gene expression pathways involved in NASH pathogenesis. Consistent with the clinical features of NASH, GAN DIO-NASH mice demonstrated key components of the metabolic syndrome, including obesity and impaired glucose tolerance. Conclusions The GAN DIO-NASH mouse model demonstrates good clinical translatability with respect to the histopathological, transcriptional and metabolic aspects of the human disease, highlighting the suitability of the GAN DIO-NASH mouse model for identifying therapeutic targets and characterizing novel drug therapies for NASH. Non-alcoholic steatohepatitis Mouse model Diet-induced obesity Translatability Histopathology Histomorphometry Diseases of the digestive system. Gastroenterology Helene M. Ægidius verfasserin aut Denise Oró verfasserin aut Simon S. Evers verfasserin aut Sara Heebøll verfasserin aut Peter Lykke Eriksen verfasserin aut Karen Louise Thomsen verfasserin aut Anja Bengtsson verfasserin aut Sanne S. Veidal verfasserin aut Michel Feigh verfasserin aut Malte P. Suppli verfasserin aut Filip K. Knop verfasserin aut Henning Grønbæk verfasserin aut Diego Miranda verfasserin aut James L. Trevaskis verfasserin aut Niels Vrang verfasserin aut Jacob Jelsing verfasserin aut Kristoffer T. G. Rigbolt verfasserin aut In BMC Gastroenterology BMC, 2003 20(2020), 1, Seite 12 (DE-627)326643702 (DE-600)2041351-8 1471230X nnns volume:20 year:2020 number:1 pages:12 https://doi.org/10.1186/s12876-020-01356-2 kostenfrei https://doaj.org/article/738511df0fdc4d36be87fd7875e0fda9 kostenfrei http://link.springer.com/article/10.1186/s12876-020-01356-2 kostenfrei https://doaj.org/toc/1471-230X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 20 2020 1 12
allfields_unstemmed	10.1186/s12876-020-01356-2 doi (DE-627)DOAJ043501761 (DE-599)DOAJ738511df0fdc4d36be87fd7875e0fda9 DE-627 ger DE-627 rakwb eng RC799-869 Henrik H. Hansen verfasserin aut Human translatability of the GAN diet-induced obese mouse model of non-alcoholic steatohepatitis 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Animal models of non-alcoholic steatohepatitis (NASH) are important tools in preclinical research and drug discovery. Gubra-Amylin NASH (GAN) diet-induced obese (DIO) mice represent a model of fibrosing NASH. The present study directly assessed the clinical translatability of the model by head-to-head comparison of liver biopsy histological and transcriptome changes in GAN DIO-NASH mouse and human NASH patients. Methods C57Bl/6 J mice were fed chow or the GAN diet rich in saturated fat (40%), fructose (22%) and cholesterol (2%) for ≥38 weeks. Metabolic parameters as well as plasma and liver biomarkers were assessed. Liver biopsy histology and transcriptome signatures were compared to samples from human lean individuals and patients diagnosed with NASH. Results Liver lesions in GAN DIO-NASH mice showed similar morphological characteristics compared to the NASH patient validation set, including macrosteatosis, lobular inflammation, hepatocyte ballooning degeneration and periportal/perisinusoidal fibrosis. Histomorphometric analysis indicated comparable increases in markers of hepatic lipid accumulation, inflammation and collagen deposition in GAN DIO-NASH mice and NASH patient samples. Liver biopsies from GAN DIO-NASH mice and NASH patients showed comparable dynamics in several gene expression pathways involved in NASH pathogenesis. Consistent with the clinical features of NASH, GAN DIO-NASH mice demonstrated key components of the metabolic syndrome, including obesity and impaired glucose tolerance. Conclusions The GAN DIO-NASH mouse model demonstrates good clinical translatability with respect to the histopathological, transcriptional and metabolic aspects of the human disease, highlighting the suitability of the GAN DIO-NASH mouse model for identifying therapeutic targets and characterizing novel drug therapies for NASH. Non-alcoholic steatohepatitis Mouse model Diet-induced obesity Translatability Histopathology Histomorphometry Diseases of the digestive system. Gastroenterology Helene M. Ægidius verfasserin aut Denise Oró verfasserin aut Simon S. Evers verfasserin aut Sara Heebøll verfasserin aut Peter Lykke Eriksen verfasserin aut Karen Louise Thomsen verfasserin aut Anja Bengtsson verfasserin aut Sanne S. Veidal verfasserin aut Michel Feigh verfasserin aut Malte P. Suppli verfasserin aut Filip K. Knop verfasserin aut Henning Grønbæk verfasserin aut Diego Miranda verfasserin aut James L. Trevaskis verfasserin aut Niels Vrang verfasserin aut Jacob Jelsing verfasserin aut Kristoffer T. G. Rigbolt verfasserin aut In BMC Gastroenterology BMC, 2003 20(2020), 1, Seite 12 (DE-627)326643702 (DE-600)2041351-8 1471230X nnns volume:20 year:2020 number:1 pages:12 https://doi.org/10.1186/s12876-020-01356-2 kostenfrei https://doaj.org/article/738511df0fdc4d36be87fd7875e0fda9 kostenfrei http://link.springer.com/article/10.1186/s12876-020-01356-2 kostenfrei https://doaj.org/toc/1471-230X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 20 2020 1 12
allfieldsGer	10.1186/s12876-020-01356-2 doi (DE-627)DOAJ043501761 (DE-599)DOAJ738511df0fdc4d36be87fd7875e0fda9 DE-627 ger DE-627 rakwb eng RC799-869 Henrik H. Hansen verfasserin aut Human translatability of the GAN diet-induced obese mouse model of non-alcoholic steatohepatitis 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Animal models of non-alcoholic steatohepatitis (NASH) are important tools in preclinical research and drug discovery. Gubra-Amylin NASH (GAN) diet-induced obese (DIO) mice represent a model of fibrosing NASH. The present study directly assessed the clinical translatability of the model by head-to-head comparison of liver biopsy histological and transcriptome changes in GAN DIO-NASH mouse and human NASH patients. Methods C57Bl/6 J mice were fed chow or the GAN diet rich in saturated fat (40%), fructose (22%) and cholesterol (2%) for ≥38 weeks. Metabolic parameters as well as plasma and liver biomarkers were assessed. Liver biopsy histology and transcriptome signatures were compared to samples from human lean individuals and patients diagnosed with NASH. Results Liver lesions in GAN DIO-NASH mice showed similar morphological characteristics compared to the NASH patient validation set, including macrosteatosis, lobular inflammation, hepatocyte ballooning degeneration and periportal/perisinusoidal fibrosis. Histomorphometric analysis indicated comparable increases in markers of hepatic lipid accumulation, inflammation and collagen deposition in GAN DIO-NASH mice and NASH patient samples. Liver biopsies from GAN DIO-NASH mice and NASH patients showed comparable dynamics in several gene expression pathways involved in NASH pathogenesis. Consistent with the clinical features of NASH, GAN DIO-NASH mice demonstrated key components of the metabolic syndrome, including obesity and impaired glucose tolerance. Conclusions The GAN DIO-NASH mouse model demonstrates good clinical translatability with respect to the histopathological, transcriptional and metabolic aspects of the human disease, highlighting the suitability of the GAN DIO-NASH mouse model for identifying therapeutic targets and characterizing novel drug therapies for NASH. Non-alcoholic steatohepatitis Mouse model Diet-induced obesity Translatability Histopathology Histomorphometry Diseases of the digestive system. Gastroenterology Helene M. Ægidius verfasserin aut Denise Oró verfasserin aut Simon S. Evers verfasserin aut Sara Heebøll verfasserin aut Peter Lykke Eriksen verfasserin aut Karen Louise Thomsen verfasserin aut Anja Bengtsson verfasserin aut Sanne S. Veidal verfasserin aut Michel Feigh verfasserin aut Malte P. Suppli verfasserin aut Filip K. Knop verfasserin aut Henning Grønbæk verfasserin aut Diego Miranda verfasserin aut James L. Trevaskis verfasserin aut Niels Vrang verfasserin aut Jacob Jelsing verfasserin aut Kristoffer T. G. Rigbolt verfasserin aut In BMC Gastroenterology BMC, 2003 20(2020), 1, Seite 12 (DE-627)326643702 (DE-600)2041351-8 1471230X nnns volume:20 year:2020 number:1 pages:12 https://doi.org/10.1186/s12876-020-01356-2 kostenfrei https://doaj.org/article/738511df0fdc4d36be87fd7875e0fda9 kostenfrei http://link.springer.com/article/10.1186/s12876-020-01356-2 kostenfrei https://doaj.org/toc/1471-230X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 20 2020 1 12
allfieldsSound	10.1186/s12876-020-01356-2 doi (DE-627)DOAJ043501761 (DE-599)DOAJ738511df0fdc4d36be87fd7875e0fda9 DE-627 ger DE-627 rakwb eng RC799-869 Henrik H. Hansen verfasserin aut Human translatability of the GAN diet-induced obese mouse model of non-alcoholic steatohepatitis 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Animal models of non-alcoholic steatohepatitis (NASH) are important tools in preclinical research and drug discovery. Gubra-Amylin NASH (GAN) diet-induced obese (DIO) mice represent a model of fibrosing NASH. The present study directly assessed the clinical translatability of the model by head-to-head comparison of liver biopsy histological and transcriptome changes in GAN DIO-NASH mouse and human NASH patients. Methods C57Bl/6 J mice were fed chow or the GAN diet rich in saturated fat (40%), fructose (22%) and cholesterol (2%) for ≥38 weeks. Metabolic parameters as well as plasma and liver biomarkers were assessed. Liver biopsy histology and transcriptome signatures were compared to samples from human lean individuals and patients diagnosed with NASH. Results Liver lesions in GAN DIO-NASH mice showed similar morphological characteristics compared to the NASH patient validation set, including macrosteatosis, lobular inflammation, hepatocyte ballooning degeneration and periportal/perisinusoidal fibrosis. Histomorphometric analysis indicated comparable increases in markers of hepatic lipid accumulation, inflammation and collagen deposition in GAN DIO-NASH mice and NASH patient samples. Liver biopsies from GAN DIO-NASH mice and NASH patients showed comparable dynamics in several gene expression pathways involved in NASH pathogenesis. Consistent with the clinical features of NASH, GAN DIO-NASH mice demonstrated key components of the metabolic syndrome, including obesity and impaired glucose tolerance. Conclusions The GAN DIO-NASH mouse model demonstrates good clinical translatability with respect to the histopathological, transcriptional and metabolic aspects of the human disease, highlighting the suitability of the GAN DIO-NASH mouse model for identifying therapeutic targets and characterizing novel drug therapies for NASH. Non-alcoholic steatohepatitis Mouse model Diet-induced obesity Translatability Histopathology Histomorphometry Diseases of the digestive system. Gastroenterology Helene M. Ægidius verfasserin aut Denise Oró verfasserin aut Simon S. Evers verfasserin aut Sara Heebøll verfasserin aut Peter Lykke Eriksen verfasserin aut Karen Louise Thomsen verfasserin aut Anja Bengtsson verfasserin aut Sanne S. Veidal verfasserin aut Michel Feigh verfasserin aut Malte P. Suppli verfasserin aut Filip K. Knop verfasserin aut Henning Grønbæk verfasserin aut Diego Miranda verfasserin aut James L. Trevaskis verfasserin aut Niels Vrang verfasserin aut Jacob Jelsing verfasserin aut Kristoffer T. G. Rigbolt verfasserin aut In BMC Gastroenterology BMC, 2003 20(2020), 1, Seite 12 (DE-627)326643702 (DE-600)2041351-8 1471230X nnns volume:20 year:2020 number:1 pages:12 https://doi.org/10.1186/s12876-020-01356-2 kostenfrei https://doaj.org/article/738511df0fdc4d36be87fd7875e0fda9 kostenfrei http://link.springer.com/article/10.1186/s12876-020-01356-2 kostenfrei https://doaj.org/toc/1471-230X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 20 2020 1 12
language	English
source	In BMC Gastroenterology 20(2020), 1, Seite 12 volume:20 year:2020 number:1 pages:12
sourceStr	In BMC Gastroenterology 20(2020), 1, Seite 12 volume:20 year:2020 number:1 pages:12
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Non-alcoholic steatohepatitis Mouse model Diet-induced obesity Translatability Histopathology Histomorphometry Diseases of the digestive system. Gastroenterology
isfreeaccess_bool	true
container_title	BMC Gastroenterology
authorswithroles_txt_mv	Henrik H. Hansen @@aut@@ Helene M. Ægidius @@aut@@ Denise Oró @@aut@@ Simon S. Evers @@aut@@ Sara Heebøll @@aut@@ Peter Lykke Eriksen @@aut@@ Karen Louise Thomsen @@aut@@ Anja Bengtsson @@aut@@ Sanne S. Veidal @@aut@@ Michel Feigh @@aut@@ Malte P. Suppli @@aut@@ Filip K. Knop @@aut@@ Henning Grønbæk @@aut@@ Diego Miranda @@aut@@ James L. Trevaskis @@aut@@ Niels Vrang @@aut@@ Jacob Jelsing @@aut@@ Kristoffer T. G. Rigbolt @@aut@@
publishDateDaySort_date	2020-01-01T00:00:00Z
hierarchy_top_id	326643702
id	DOAJ043501761
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ043501761</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230503150324.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230227s2020 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/s12876-020-01356-2</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ043501761</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ738511df0fdc4d36be87fd7875e0fda9</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC799-869</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Henrik H. Hansen</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Human translatability of the GAN diet-induced obese mouse model of non-alcoholic steatohepatitis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2020</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Background Animal models of non-alcoholic steatohepatitis (NASH) are important tools in preclinical research and drug discovery. Gubra-Amylin NASH (GAN) diet-induced obese (DIO) mice represent a model of fibrosing NASH. The present study directly assessed the clinical translatability of the model by head-to-head comparison of liver biopsy histological and transcriptome changes in GAN DIO-NASH mouse and human NASH patients. Methods C57Bl/6 J mice were fed chow or the GAN diet rich in saturated fat (40%), fructose (22%) and cholesterol (2%) for ≥38 weeks. Metabolic parameters as well as plasma and liver biomarkers were assessed. Liver biopsy histology and transcriptome signatures were compared to samples from human lean individuals and patients diagnosed with NASH. Results Liver lesions in GAN DIO-NASH mice showed similar morphological characteristics compared to the NASH patient validation set, including macrosteatosis, lobular inflammation, hepatocyte ballooning degeneration and periportal/perisinusoidal fibrosis. Histomorphometric analysis indicated comparable increases in markers of hepatic lipid accumulation, inflammation and collagen deposition in GAN DIO-NASH mice and NASH patient samples. Liver biopsies from GAN DIO-NASH mice and NASH patients showed comparable dynamics in several gene expression pathways involved in NASH pathogenesis. Consistent with the clinical features of NASH, GAN DIO-NASH mice demonstrated key components of the metabolic syndrome, including obesity and impaired glucose tolerance. Conclusions The GAN DIO-NASH mouse model demonstrates good clinical translatability with respect to the histopathological, transcriptional and metabolic aspects of the human disease, highlighting the suitability of the GAN DIO-NASH mouse model for identifying therapeutic targets and characterizing novel drug therapies for NASH.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Non-alcoholic steatohepatitis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Mouse model</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Diet-induced obesity</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Translatability</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Histopathology</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Histomorphometry</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Diseases of the digestive system. Gastroenterology</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Helene M. Ægidius</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Denise Oró</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Simon S. 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callnumber-first	R - Medicine
author	Henrik H. Hansen
spellingShingle	Henrik H. Hansen misc RC799-869 misc Non-alcoholic steatohepatitis misc Mouse model misc Diet-induced obesity misc Translatability misc Histopathology misc Histomorphometry misc Diseases of the digestive system. Gastroenterology Human translatability of the GAN diet-induced obese mouse model of non-alcoholic steatohepatitis
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topic_title	RC799-869 Human translatability of the GAN diet-induced obese mouse model of non-alcoholic steatohepatitis Non-alcoholic steatohepatitis Mouse model Diet-induced obesity Translatability Histopathology Histomorphometry
topic	misc RC799-869 misc Non-alcoholic steatohepatitis misc Mouse model misc Diet-induced obesity misc Translatability misc Histopathology misc Histomorphometry misc Diseases of the digestive system. Gastroenterology
topic_unstemmed	misc RC799-869 misc Non-alcoholic steatohepatitis misc Mouse model misc Diet-induced obesity misc Translatability misc Histopathology misc Histomorphometry misc Diseases of the digestive system. Gastroenterology
topic_browse	misc RC799-869 misc Non-alcoholic steatohepatitis misc Mouse model misc Diet-induced obesity misc Translatability misc Histopathology misc Histomorphometry misc Diseases of the digestive system. Gastroenterology
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title	Human translatability of the GAN diet-induced obese mouse model of non-alcoholic steatohepatitis
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title_full	Human translatability of the GAN diet-induced obese mouse model of non-alcoholic steatohepatitis
author_sort	Henrik H. Hansen
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author_browse	Henrik H. Hansen Helene M. Ægidius Denise Oró Simon S. Evers Sara Heebøll Peter Lykke Eriksen Karen Louise Thomsen Anja Bengtsson Sanne S. Veidal Michel Feigh Malte P. Suppli Filip K. Knop Henning Grønbæk Diego Miranda James L. Trevaskis Niels Vrang Jacob Jelsing Kristoffer T. G. Rigbolt
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title_sort	human translatability of the gan diet-induced obese mouse model of non-alcoholic steatohepatitis
callnumber	RC799-869
title_auth	Human translatability of the GAN diet-induced obese mouse model of non-alcoholic steatohepatitis
abstract	Abstract Background Animal models of non-alcoholic steatohepatitis (NASH) are important tools in preclinical research and drug discovery. Gubra-Amylin NASH (GAN) diet-induced obese (DIO) mice represent a model of fibrosing NASH. The present study directly assessed the clinical translatability of the model by head-to-head comparison of liver biopsy histological and transcriptome changes in GAN DIO-NASH mouse and human NASH patients. Methods C57Bl/6 J mice were fed chow or the GAN diet rich in saturated fat (40%), fructose (22%) and cholesterol (2%) for ≥38 weeks. Metabolic parameters as well as plasma and liver biomarkers were assessed. Liver biopsy histology and transcriptome signatures were compared to samples from human lean individuals and patients diagnosed with NASH. Results Liver lesions in GAN DIO-NASH mice showed similar morphological characteristics compared to the NASH patient validation set, including macrosteatosis, lobular inflammation, hepatocyte ballooning degeneration and periportal/perisinusoidal fibrosis. Histomorphometric analysis indicated comparable increases in markers of hepatic lipid accumulation, inflammation and collagen deposition in GAN DIO-NASH mice and NASH patient samples. Liver biopsies from GAN DIO-NASH mice and NASH patients showed comparable dynamics in several gene expression pathways involved in NASH pathogenesis. Consistent with the clinical features of NASH, GAN DIO-NASH mice demonstrated key components of the metabolic syndrome, including obesity and impaired glucose tolerance. Conclusions The GAN DIO-NASH mouse model demonstrates good clinical translatability with respect to the histopathological, transcriptional and metabolic aspects of the human disease, highlighting the suitability of the GAN DIO-NASH mouse model for identifying therapeutic targets and characterizing novel drug therapies for NASH.
abstractGer	Abstract Background Animal models of non-alcoholic steatohepatitis (NASH) are important tools in preclinical research and drug discovery. Gubra-Amylin NASH (GAN) diet-induced obese (DIO) mice represent a model of fibrosing NASH. The present study directly assessed the clinical translatability of the model by head-to-head comparison of liver biopsy histological and transcriptome changes in GAN DIO-NASH mouse and human NASH patients. Methods C57Bl/6 J mice were fed chow or the GAN diet rich in saturated fat (40%), fructose (22%) and cholesterol (2%) for ≥38 weeks. Metabolic parameters as well as plasma and liver biomarkers were assessed. Liver biopsy histology and transcriptome signatures were compared to samples from human lean individuals and patients diagnosed with NASH. Results Liver lesions in GAN DIO-NASH mice showed similar morphological characteristics compared to the NASH patient validation set, including macrosteatosis, lobular inflammation, hepatocyte ballooning degeneration and periportal/perisinusoidal fibrosis. Histomorphometric analysis indicated comparable increases in markers of hepatic lipid accumulation, inflammation and collagen deposition in GAN DIO-NASH mice and NASH patient samples. Liver biopsies from GAN DIO-NASH mice and NASH patients showed comparable dynamics in several gene expression pathways involved in NASH pathogenesis. Consistent with the clinical features of NASH, GAN DIO-NASH mice demonstrated key components of the metabolic syndrome, including obesity and impaired glucose tolerance. Conclusions The GAN DIO-NASH mouse model demonstrates good clinical translatability with respect to the histopathological, transcriptional and metabolic aspects of the human disease, highlighting the suitability of the GAN DIO-NASH mouse model for identifying therapeutic targets and characterizing novel drug therapies for NASH.
abstract_unstemmed	Abstract Background Animal models of non-alcoholic steatohepatitis (NASH) are important tools in preclinical research and drug discovery. Gubra-Amylin NASH (GAN) diet-induced obese (DIO) mice represent a model of fibrosing NASH. The present study directly assessed the clinical translatability of the model by head-to-head comparison of liver biopsy histological and transcriptome changes in GAN DIO-NASH mouse and human NASH patients. Methods C57Bl/6 J mice were fed chow or the GAN diet rich in saturated fat (40%), fructose (22%) and cholesterol (2%) for ≥38 weeks. Metabolic parameters as well as plasma and liver biomarkers were assessed. Liver biopsy histology and transcriptome signatures were compared to samples from human lean individuals and patients diagnosed with NASH. Results Liver lesions in GAN DIO-NASH mice showed similar morphological characteristics compared to the NASH patient validation set, including macrosteatosis, lobular inflammation, hepatocyte ballooning degeneration and periportal/perisinusoidal fibrosis. Histomorphometric analysis indicated comparable increases in markers of hepatic lipid accumulation, inflammation and collagen deposition in GAN DIO-NASH mice and NASH patient samples. Liver biopsies from GAN DIO-NASH mice and NASH patients showed comparable dynamics in several gene expression pathways involved in NASH pathogenesis. Consistent with the clinical features of NASH, GAN DIO-NASH mice demonstrated key components of the metabolic syndrome, including obesity and impaired glucose tolerance. Conclusions The GAN DIO-NASH mouse model demonstrates good clinical translatability with respect to the histopathological, transcriptional and metabolic aspects of the human disease, highlighting the suitability of the GAN DIO-NASH mouse model for identifying therapeutic targets and characterizing novel drug therapies for NASH.
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title_short	Human translatability of the GAN diet-induced obese mouse model of non-alcoholic steatohepatitis
url	https://doi.org/10.1186/s12876-020-01356-2 https://doaj.org/article/738511df0fdc4d36be87fd7875e0fda9 http://link.springer.com/article/10.1186/s12876-020-01356-2 https://doaj.org/toc/1471-230X
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author2Str	Helene M. Ægidius Denise Oró Simon S. Evers Sara Heebøll Peter Lykke Eriksen Karen Louise Thomsen Anja Bengtsson Sanne S. Veidal Michel Feigh Malte P. Suppli Filip K. Knop Henning Grønbæk Diego Miranda James L. Trevaskis Niels Vrang Jacob Jelsing Kristoffer T. G. Rigbolt
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Hansen</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Human translatability of the GAN diet-induced obese mouse model of non-alcoholic steatohepatitis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2020</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Background Animal models of non-alcoholic steatohepatitis (NASH) are important tools in preclinical research and drug discovery. Gubra-Amylin NASH (GAN) diet-induced obese (DIO) mice represent a model of fibrosing NASH. The present study directly assessed the clinical translatability of the model by head-to-head comparison of liver biopsy histological and transcriptome changes in GAN DIO-NASH mouse and human NASH patients. Methods C57Bl/6 J mice were fed chow or the GAN diet rich in saturated fat (40%), fructose (22%) and cholesterol (2%) for ≥38 weeks. Metabolic parameters as well as plasma and liver biomarkers were assessed. Liver biopsy histology and transcriptome signatures were compared to samples from human lean individuals and patients diagnosed with NASH. Results Liver lesions in GAN DIO-NASH mice showed similar morphological characteristics compared to the NASH patient validation set, including macrosteatosis, lobular inflammation, hepatocyte ballooning degeneration and periportal/perisinusoidal fibrosis. Histomorphometric analysis indicated comparable increases in markers of hepatic lipid accumulation, inflammation and collagen deposition in GAN DIO-NASH mice and NASH patient samples. Liver biopsies from GAN DIO-NASH mice and NASH patients showed comparable dynamics in several gene expression pathways involved in NASH pathogenesis. Consistent with the clinical features of NASH, GAN DIO-NASH mice demonstrated key components of the metabolic syndrome, including obesity and impaired glucose tolerance. Conclusions The GAN DIO-NASH mouse model demonstrates good clinical translatability with respect to the histopathological, transcriptional and metabolic aspects of the human disease, highlighting the suitability of the GAN DIO-NASH mouse model for identifying therapeutic targets and characterizing novel drug therapies for NASH.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Non-alcoholic steatohepatitis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Mouse model</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Diet-induced obesity</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Translatability</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Histopathology</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Histomorphometry</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Diseases of the digestive system. 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Evers</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Sara Heebøll</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Peter Lykke Eriksen</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Karen Louise Thomsen</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Anja Bengtsson</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Sanne S. 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Human translatability of the GAN diet-induced obese mouse model of non-alcoholic steatohepatitis

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