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The present study aimed to evaluate the joint action of a high-fat diet and CCl4 in developing a short-term non-alcoholic steatohepatitis model. C57BL6\/J mice were divided into two groups: standard diet-fed (SD), the high-fat diet-fed (HFD) and HFD + fructose-fed and carbon tetrachloride (HFD+CCl4). The animals fed with HFD+CCl4 presented increased lipid deposition compared with both SD and HFD mice. Plasma cholesterol was increased in animals from the HFD+CCl4 group compared with the SD and HFD groups, without significant differences between the SD and HFD groups. Plasma triglycerides showed no significant difference between the groups. The HFD+CCl4 animals had increased collagen deposition in the liver compared with both SD and HFD groups. Hydroxyproline was also increased in the HFD+CCl4 group. Liver enzymes, alanine aminotransferase and aspartate aminotransferase, were increased in the HFD+CCl4 group, compared with SD and HFD groups. Also, CCl4 was able to trigger an inflammatory process in the liver of HFD-fed animals by promoting an increase of \u223c2 times in macrophage activity, \u223c6 times in F4\/80 gene expression, and pro-inflammatory cytokines (IL-1b and TNFa), in addition to an increase in inflammatory pathway protein phosphorylation (IKKbp). HFD e HFD+CCl4 animals increased glucose intolerance compared with SD mice, associated with reduced insulin-stimulated AKT activity in the liver. Therefore, our study has shown that short-term HFD feeding associated with fructose and CCl4 can trigger non-alcoholic steatohepatitis and cause damage to glucose metabolism.<\/jats:p>","DOI":"10.1042\/bsr20231532","type":"journal-article","created":{"date-parts":[[2024,4,25]],"date-time":"2024-04-25T10:39:00Z","timestamp":1714041540000},"update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["A short-term rodent model for non-alcoholic steatohepatitis induced by a high-fat diet and carbon tetrachloride"],"prefix":"10.1042","volume":"44","author":[{"given":"Layanne\u00a0C.C.","family":"Araujo","sequence":"first","affiliation":[{"name":"1Department of Physiology, Ribeirao Preto School of Medicine, University of Sao Paulo, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carolina\u00a0C.B.","family":"Dias","sequence":"additional","affiliation":[{"name":"1Department of Physiology, Ribeirao Preto School of Medicine, University of Sao Paulo, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Felipe\u00a0G.","family":"Sucupira","sequence":"additional","affiliation":[{"name":"1Department of Physiology, Ribeirao Preto School of Medicine, University of Sao Paulo, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leandra\u00a0N.Z.","family":"Ramalho","sequence":"additional","affiliation":[{"name":"2Department of Pathology and Legal Medicine, Ribeirao Preto School of Medicine, University of Sao Paulo, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3486-4301","authenticated-orcid":false,"given":"Jo\u00e3o\u00a0Paulo","family":"Camporez","sequence":"additional","affiliation":[{"name":"1Department of Physiology, Ribeirao Preto School of Medicine, University of Sao Paulo, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2024,5,8]]},"reference":[{"key":"2024050806554820000_B1","doi-asserted-by":"publisher","first-page":"713","DOI":"10.1002\/hep.26672","article-title":"Nonalcoholic fatty liver disease, hepatic insulin resistance, and type 2 diabetes","volume":"59","author":"Birkenfeld","year":"2014","journal-title":"Hepatology"},{"key":"2024050806554820000_B2","doi-asserted-by":"publisher","first-page":"526","DOI":"10.1194\/jlr.M054080","article-title":"ApoA5 knockdown improves whole-body insulin sensitivity in high-fat-fed mice by reducing ectopic lipid content","volume":"56","author":"Camporez","year":"2015","journal-title":"J. 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