Analysis of amino acid profiles of blood over time and biomarkers associated with non-alcoholic steatohepatitis in STAM mice
The changes in free amino acid (AA) levels in blood during the progression from non-alcoholic steatohepatitis (NASH) to hepatocellular carcinoma (HCC) are unclear. We investigated serum AA levels, along with biochemical and histological events, in a mouse model of NASH. We induced NASH in male C57BL...
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| Veröffentlicht in: | Experimental Animals 2019, Vol.68(4), pp.417-428 |
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| creator | Iida, Ayaka Kuranuki, Sachi Yamamoto, Ryoko Uchida, Masaya Ohta, Masanori Ichimura, Mayuko Tsuneyama, Koichi Masaki, Takayuki Seike, Masataka Nakamura, Tsuyoshi |
| description | The changes in free amino acid (AA) levels in blood during the progression from non-alcoholic steatohepatitis (NASH) to hepatocellular carcinoma (HCC) are unclear. We investigated serum AA levels, along with biochemical and histological events, in a mouse model of NASH. We induced NASH in male C57BL/6J mice with a streptozotocin injection and high-fat diet after 4 weeks of age (STAM group). We chronologically (6, 8, 10, 12, and 16 weeks, n=4–12 mice/group) evaluated the progression from steatohepatitis to HCC by biochemical and histological analyses. The serum AA levels were determined using an AA analyzer. Serum aspartate aminotransferase and alanine aminotransferase levels were higher in the STAM group than in the normal group (non-NASH-induced mice). Histological analysis revealed that STAM mice had fatty liver, NASH, and fibrosis at 6, 8, and 10 weeks, respectively. Moreover, the mice exhibited fibrosis and HCC at 16 weeks. The serum branched-chain AA levels were higher in the STAM group than in the normal group, especially at 8 and 10 weeks. The Fischer ratio decreased at 16 weeks in the STAM group, with increasing aromatic AA levels. These results suggested that this model sequentially depicts the development of fatty liver, NASH, cirrhosis, HCC, and AA metabolism disorders within a short experimental period. Additionally, serum amyloid A was suggested to be a useful inflammation biomarker associated with NASH. We believe that the STAM model will be useful for studying AA metabolism and/or pharmacological effects in NASH. |
| doi_str_mv | 10.1538/expanim.18-0152 |
| format | Article |
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We investigated serum AA levels, along with biochemical and histological events, in a mouse model of NASH. We induced NASH in male C57BL/6J mice with a streptozotocin injection and high-fat diet after 4 weeks of age (STAM group). We chronologically (6, 8, 10, 12, and 16 weeks, n=4–12 mice/group) evaluated the progression from steatohepatitis to HCC by biochemical and histological analyses. The serum AA levels were determined using an AA analyzer. Serum aspartate aminotransferase and alanine aminotransferase levels were higher in the STAM group than in the normal group (non-NASH-induced mice). Histological analysis revealed that STAM mice had fatty liver, NASH, and fibrosis at 6, 8, and 10 weeks, respectively. Moreover, the mice exhibited fibrosis and HCC at 16 weeks. The serum branched-chain AA levels were higher in the STAM group than in the normal group, especially at 8 and 10 weeks. The Fischer ratio decreased at 16 weeks in the STAM group, with increasing aromatic AA levels. These results suggested that this model sequentially depicts the development of fatty liver, NASH, cirrhosis, HCC, and AA metabolism disorders within a short experimental period. Additionally, serum amyloid A was suggested to be a useful inflammation biomarker associated with NASH. We believe that the STAM model will be useful for studying AA metabolism and/or pharmacological effects in NASH.</description><identifier>ISSN: 1341-1357</identifier><identifier>EISSN: 1881-7122</identifier><identifier>DOI: 10.1538/expanim.18-0152</identifier><identifier>PMID: 31155606</identifier><language>eng</language><publisher>Japan: Japanese Association for Laboratory Animal Science</publisher><subject>Alanine ; Alanine transaminase ; amino acid metabolism disorder ; Amino acid sequence ; Amino Acids - blood ; Amyloid ; Animals ; Aspartate aminotransferase ; Biomarkers ; Biomarkers - metabolism ; Blood ; Carcinoma, Hepatocellular - blood ; Carcinoma, Hepatocellular - etiology ; Carcinoma, Hepatocellular - metabolism ; Chain branching ; Cirrhosis ; diabetes ; Diet, High-Fat - adverse effects ; Disease Models, Animal ; Fatty liver ; Fibrosis ; Hepatocellular carcinoma ; High fat diet ; hyperlipidemia ; Liver ; Liver cirrhosis ; Male ; Metabolism ; Mice ; Mice, Inbred C57BL ; non-alcoholic fatty liver disease ; Non-alcoholic Fatty Liver Disease - blood ; Non-alcoholic Fatty Liver Disease - etiology ; Non-alcoholic Fatty Liver Disease - metabolism ; non-alcoholic steatohepatitis ; Original ; Serum - chemistry ; Streptozocin ; Streptozocin - pharmacology ; Time Factors</subject><ispartof>Experimental Animals, 2019, Vol.68(4), pp.417-428</ispartof><rights>2019 Japanese Association for Laboratory Animal Science</rights><rights>Copyright Japan Science and Technology Agency 2019</rights><rights>2019 Japanese Association for Laboratory Animal Science 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c573t-2dc3d317bd19482ef2130ff8a8352fa38d31b44ffdc24d1607da049c517d70283</citedby><cites>FETCH-LOGICAL-c573t-2dc3d317bd19482ef2130ff8a8352fa38d31b44ffdc24d1607da049c517d70283</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6842803/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6842803/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,1883,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31155606$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Iida, Ayaka</creatorcontrib><creatorcontrib>Kuranuki, Sachi</creatorcontrib><creatorcontrib>Yamamoto, Ryoko</creatorcontrib><creatorcontrib>Uchida, Masaya</creatorcontrib><creatorcontrib>Ohta, Masanori</creatorcontrib><creatorcontrib>Ichimura, Mayuko</creatorcontrib><creatorcontrib>Tsuneyama, Koichi</creatorcontrib><creatorcontrib>Masaki, Takayuki</creatorcontrib><creatorcontrib>Seike, Masataka</creatorcontrib><creatorcontrib>Nakamura, Tsuyoshi</creatorcontrib><title>Analysis of amino acid profiles of blood over time and biomarkers associated with non-alcoholic steatohepatitis in STAM mice</title><title>Experimental Animals</title><addtitle>Exp Anim</addtitle><description>The changes in free amino acid (AA) levels in blood during the progression from non-alcoholic steatohepatitis (NASH) to hepatocellular carcinoma (HCC) are unclear. We investigated serum AA levels, along with biochemical and histological events, in a mouse model of NASH. We induced NASH in male C57BL/6J mice with a streptozotocin injection and high-fat diet after 4 weeks of age (STAM group). We chronologically (6, 8, 10, 12, and 16 weeks, n=4–12 mice/group) evaluated the progression from steatohepatitis to HCC by biochemical and histological analyses. The serum AA levels were determined using an AA analyzer. Serum aspartate aminotransferase and alanine aminotransferase levels were higher in the STAM group than in the normal group (non-NASH-induced mice). Histological analysis revealed that STAM mice had fatty liver, NASH, and fibrosis at 6, 8, and 10 weeks, respectively. Moreover, the mice exhibited fibrosis and HCC at 16 weeks. The serum branched-chain AA levels were higher in the STAM group than in the normal group, especially at 8 and 10 weeks. The Fischer ratio decreased at 16 weeks in the STAM group, with increasing aromatic AA levels. These results suggested that this model sequentially depicts the development of fatty liver, NASH, cirrhosis, HCC, and AA metabolism disorders within a short experimental period. Additionally, serum amyloid A was suggested to be a useful inflammation biomarker associated with NASH. We believe that the STAM model will be useful for studying AA metabolism and/or pharmacological effects in NASH.</description><subject>Alanine</subject><subject>Alanine transaminase</subject><subject>amino acid metabolism disorder</subject><subject>Amino acid sequence</subject><subject>Amino Acids - blood</subject><subject>Amyloid</subject><subject>Animals</subject><subject>Aspartate aminotransferase</subject><subject>Biomarkers</subject><subject>Biomarkers - metabolism</subject><subject>Blood</subject><subject>Carcinoma, Hepatocellular - blood</subject><subject>Carcinoma, Hepatocellular - etiology</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Chain branching</subject><subject>Cirrhosis</subject><subject>diabetes</subject><subject>Diet, High-Fat - adverse effects</subject><subject>Disease Models, Animal</subject><subject>Fatty liver</subject><subject>Fibrosis</subject><subject>Hepatocellular carcinoma</subject><subject>High fat diet</subject><subject>hyperlipidemia</subject><subject>Liver</subject><subject>Liver cirrhosis</subject><subject>Male</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>non-alcoholic fatty liver disease</subject><subject>Non-alcoholic Fatty Liver Disease - blood</subject><subject>Non-alcoholic Fatty Liver Disease - etiology</subject><subject>Non-alcoholic Fatty Liver Disease - metabolism</subject><subject>non-alcoholic steatohepatitis</subject><subject>Original</subject><subject>Serum - chemistry</subject><subject>Streptozocin</subject><subject>Streptozocin - pharmacology</subject><subject>Time Factors</subject><issn>1341-1357</issn><issn>1881-7122</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc1v1DAQxSMEoqVw5oYscU7rsZPYe0FaVYUiFXGgnK2JPxovib3Y3pZK_PHNsksEF4_l9_Mbj19VvQV6Di2XF_bXFoOfzkHWFFr2rDoFKaEWwNjzec8bqIG34qR6lfOGUiYEW72sTjhA23a0O61-rwOOj9lnEh3ByYdIUHtDtik6P9o_x_0YoyHx3iZS_GQJBkN6HydMP2zKBHOO2mOxhjz4MpAQQ42jjkMcvSa5WCxxsFssvsxtfCDfbtdfyOS1fV29cDhm--ZYz6rvH69uL6_rm6-fPl-ub2rdCl5qZjQ3HERvYNVIZh0DTp2TKHnLHHI5i33TOGc0awx0VBikzUq3IIygTPKz6sPBd7vrJ2u0DSXhqLbJzzM8qohe_a8EP6i7eK862TBJ-Wzw_miQ4s-dzUVt4i7NP5cV4wy6tpOdmKmLA6VTzDlZt3QAqvZxqWNcCqTaxzXfePfvwxb-bz4zcHUANrngnV0ATMXr0S6GnVTNfjkaL7oeMCkb-BOVt64n</recordid><startdate>20190101</startdate><enddate>20190101</enddate><creator>Iida, Ayaka</creator><creator>Kuranuki, Sachi</creator><creator>Yamamoto, Ryoko</creator><creator>Uchida, Masaya</creator><creator>Ohta, Masanori</creator><creator>Ichimura, Mayuko</creator><creator>Tsuneyama, Koichi</creator><creator>Masaki, Takayuki</creator><creator>Seike, Masataka</creator><creator>Nakamura, Tsuyoshi</creator><general>Japanese Association for Laboratory Animal Science</general><general>Japan Science and Technology Agency</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20190101</creationdate><title>Analysis of amino acid profiles of blood over time and biomarkers associated with non-alcoholic steatohepatitis in STAM mice</title><author>Iida, Ayaka ; Kuranuki, Sachi ; Yamamoto, Ryoko ; Uchida, Masaya ; Ohta, Masanori ; Ichimura, Mayuko ; Tsuneyama, Koichi ; Masaki, Takayuki ; Seike, Masataka ; Nakamura, Tsuyoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c573t-2dc3d317bd19482ef2130ff8a8352fa38d31b44ffdc24d1607da049c517d70283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Alanine</topic><topic>Alanine transaminase</topic><topic>amino acid metabolism disorder</topic><topic>Amino acid sequence</topic><topic>Amino Acids - blood</topic><topic>Amyloid</topic><topic>Animals</topic><topic>Aspartate aminotransferase</topic><topic>Biomarkers</topic><topic>Biomarkers - metabolism</topic><topic>Blood</topic><topic>Carcinoma, Hepatocellular - blood</topic><topic>Carcinoma, Hepatocellular - etiology</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Chain branching</topic><topic>Cirrhosis</topic><topic>diabetes</topic><topic>Diet, High-Fat - adverse effects</topic><topic>Disease Models, Animal</topic><topic>Fatty liver</topic><topic>Fibrosis</topic><topic>Hepatocellular carcinoma</topic><topic>High fat diet</topic><topic>hyperlipidemia</topic><topic>Liver</topic><topic>Liver cirrhosis</topic><topic>Male</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>non-alcoholic fatty liver disease</topic><topic>Non-alcoholic Fatty Liver Disease - blood</topic><topic>Non-alcoholic Fatty Liver Disease - etiology</topic><topic>Non-alcoholic Fatty Liver Disease - metabolism</topic><topic>non-alcoholic steatohepatitis</topic><topic>Original</topic><topic>Serum - chemistry</topic><topic>Streptozocin</topic><topic>Streptozocin - pharmacology</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Iida, Ayaka</creatorcontrib><creatorcontrib>Kuranuki, Sachi</creatorcontrib><creatorcontrib>Yamamoto, Ryoko</creatorcontrib><creatorcontrib>Uchida, Masaya</creatorcontrib><creatorcontrib>Ohta, Masanori</creatorcontrib><creatorcontrib>Ichimura, Mayuko</creatorcontrib><creatorcontrib>Tsuneyama, Koichi</creatorcontrib><creatorcontrib>Masaki, Takayuki</creatorcontrib><creatorcontrib>Seike, Masataka</creatorcontrib><creatorcontrib>Nakamura, Tsuyoshi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Experimental Animals</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Iida, Ayaka</au><au>Kuranuki, Sachi</au><au>Yamamoto, Ryoko</au><au>Uchida, Masaya</au><au>Ohta, Masanori</au><au>Ichimura, Mayuko</au><au>Tsuneyama, Koichi</au><au>Masaki, Takayuki</au><au>Seike, Masataka</au><au>Nakamura, Tsuyoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Analysis of amino acid profiles of blood over time and biomarkers associated with non-alcoholic steatohepatitis in STAM mice</atitle><jtitle>Experimental Animals</jtitle><addtitle>Exp Anim</addtitle><date>2019-01-01</date><risdate>2019</risdate><volume>68</volume><issue>4</issue><spage>417</spage><epage>428</epage><pages>417-428</pages><issn>1341-1357</issn><eissn>1881-7122</eissn><abstract>The changes in free amino acid (AA) levels in blood during the progression from non-alcoholic steatohepatitis (NASH) to hepatocellular carcinoma (HCC) are unclear. We investigated serum AA levels, along with biochemical and histological events, in a mouse model of NASH. We induced NASH in male C57BL/6J mice with a streptozotocin injection and high-fat diet after 4 weeks of age (STAM group). We chronologically (6, 8, 10, 12, and 16 weeks, n=4–12 mice/group) evaluated the progression from steatohepatitis to HCC by biochemical and histological analyses. The serum AA levels were determined using an AA analyzer. Serum aspartate aminotransferase and alanine aminotransferase levels were higher in the STAM group than in the normal group (non-NASH-induced mice). Histological analysis revealed that STAM mice had fatty liver, NASH, and fibrosis at 6, 8, and 10 weeks, respectively. Moreover, the mice exhibited fibrosis and HCC at 16 weeks. The serum branched-chain AA levels were higher in the STAM group than in the normal group, especially at 8 and 10 weeks. The Fischer ratio decreased at 16 weeks in the STAM group, with increasing aromatic AA levels. These results suggested that this model sequentially depicts the development of fatty liver, NASH, cirrhosis, HCC, and AA metabolism disorders within a short experimental period. Additionally, serum amyloid A was suggested to be a useful inflammation biomarker associated with NASH. We believe that the STAM model will be useful for studying AA metabolism and/or pharmacological effects in NASH.</abstract><cop>Japan</cop><pub>Japanese Association for Laboratory Animal Science</pub><pmid>31155606</pmid><doi>10.1538/expanim.18-0152</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Alanine Alanine transaminase amino acid metabolism disorder Amino acid sequence Amino Acids - blood Amyloid Animals Aspartate aminotransferase Biomarkers Biomarkers - metabolism Blood Carcinoma, Hepatocellular - blood Carcinoma, Hepatocellular - etiology Carcinoma, Hepatocellular - metabolism Chain branching Cirrhosis diabetes Diet, High-Fat - adverse effects Disease Models, Animal Fatty liver Fibrosis Hepatocellular carcinoma High fat diet hyperlipidemia Liver Liver cirrhosis Male Metabolism Mice Mice, Inbred C57BL non-alcoholic fatty liver disease Non-alcoholic Fatty Liver Disease - blood Non-alcoholic Fatty Liver Disease - etiology Non-alcoholic Fatty Liver Disease - metabolism non-alcoholic steatohepatitis Original Serum - chemistry Streptozocin Streptozocin - pharmacology Time Factors |
| title | Analysis of amino acid profiles of blood over time and biomarkers associated with non-alcoholic steatohepatitis in STAM mice |
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