{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T06:13:53Z","timestamp":1790662433272,"version":"4.1.0"},"reference-count":37,"publisher":"Springer Science and Business Media LLC","issue":"1","content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Lipids Health Dis"],"published-print":{"date-parts":[[2011,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Nonalcoholic fatty liver disease (NAFLD) is one of the most frequent causes of abnormal liver function. Because fatty acids can damage biological membranes, fatty acid accumulation in the liver may be partially responsible for the functional and morphological changes that are observed in nonalcoholic liver disease. The aim of this study was to use gas chromatography-mass spectrometry to evaluate the fatty acid composition of an experimental mouse model of NAFLD induced by high-fat feed and CCl\n                      <jats:sub>4<\/jats:sub>\n                      and to assess the association between liver fatty acid accumulation and NAFLD. C57BL\/6J mice were given high-fat feed for six consecutive weeks to develop experimental NAFLD. Meanwhile, these mice were given subcutaneous injections of a 40% CCl\n                      <jats:sub>4<\/jats:sub>\n                      -vegetable oil mixture twice per week.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      A pathological examination found that NAFLD had developed in the C57BL\/6J mice. High-fat feed and CCl\n                      <jats:sub>4<\/jats:sub>\n                      led to significant increases in C14:0, C16:0, C18:0 and C20:3 (P &lt; 0.01), and decreases in C15:0, C18:1, C18:2 and C18:3 (P &lt; 0.01) in the mouse liver. The treatment also led to an increase in SFA and decreases in other fatty acids (UFA, PUFA and MUFA). An increase in the ratio of product\/precursor n-6 (C20:4\/C18:2) and n-3 ([C20:5+C22:6]\/C18:3) and a decrease in the ratio of n-6\/n-3 (C20:4\/[C20:5+C22:6]) were also observed.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      These data are consistent with the hypothesis that fatty acids are deranged in mice with non-alcoholic fatty liver injury induced by high-fat feed and CCl\n                      <jats:sub>4<\/jats:sub>\n                      , which may be involved in its pathogenesis and\/or progression via an unclear mechanism.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/1476-511x-10-234","type":"journal-article","created":{"date-parts":[[2011,12,14]],"date-time":"2011-12-14T14:14:15Z","timestamp":1323872055000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":66,"title":["Liver fatty acid composition in mice with or without nonalcoholic fatty liver disease"],"prefix":"10.1186","volume":"10","author":[{"given":"Xin","family":"Wang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuzhen","family":"Cao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yunwei","family":"Fu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guifang","family":"Guo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiuying","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2011,12,14]]},"reference":[{"key":"617_CR1","doi-asserted-by":"publisher","first-page":"1","DOI":"10.1016\/j.plipres.2008.08.001","volume":"48","author":"G Musso","year":"2009","unstructured":"Musso G, Gambino R, Cassader M: Recent insights into hepatic lipid metabolism in non-alcoholic fatty liver disease(NAFLD). 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