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We aimed to investigate the roles of hepatic <jats:styled-content style=\"fixed-case\">RALDH<\/jats:styled-content>1 induction in glucose metabolism impairment using mice fed with high\u2010fat\u2010diet (<jats:styled-content style=\"fixed-case\">HFD<\/jats:styled-content>). Mice were fed with <jats:styled-content style=\"fixed-case\">HFD<\/jats:styled-content> for 8 weeks and treated with <jats:styled-content style=\"fixed-case\">RALDH<\/jats:styled-content> inhibitor citral for another 4 weeks. Oral glucose tolerance test (<jats:styled-content style=\"fixed-case\">OGTT<\/jats:styled-content>), pyruvate tolerance test (<jats:styled-content style=\"fixed-case\">PTT<\/jats:styled-content>) and insulin tolerance test were performed. Expressions of phosphoenolpyruvate carboxykinase 1 (<jats:styled-content style=\"fixed-case\">PCK<\/jats:styled-content>1), glucokinase (<jats:styled-content style=\"fixed-case\">GCK<\/jats:styled-content>) and <jats:styled-content style=\"fixed-case\">RALDH<\/jats:styled-content>1 were measured. Therapeutic effects of citral were also documented in diabetic rats. Effects of retinaldehyde on <jats:styled-content style=\"fixed-case\">PCK<\/jats:styled-content>1 and <jats:styled-content style=\"fixed-case\">GCK<\/jats:styled-content> expressions were examined in rat primary hepatocytes and HepG2 cells. The results showed that <jats:styled-content style=\"fixed-case\">HFD<\/jats:styled-content> mice were characterized by hyperlipidaemia and insulin resistance, accompanied by significantly increased <jats:styled-content style=\"fixed-case\">RALDH<\/jats:styled-content>1 activity and expression. Citral (10 and 50 mg\/kg) ameliorated <jats:styled-content style=\"fixed-case\">HFD<\/jats:styled-content>\u2010induced hyperlipidaemia and insulin resistance, as demonstrated by the improved fasting glucose, insulin levels and lipid profiles. <jats:styled-content style=\"fixed-case\">OGTT<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">PTT<\/jats:styled-content> demonstrated that citral reversed <jats:styled-content style=\"fixed-case\">HFD<\/jats:styled-content>\u2010induced glucose disposal impairment and glucose production enhancement. Citral also reversed the increased <jats:styled-content style=\"fixed-case\">PCK<\/jats:styled-content>1 expression and decreased <jats:styled-content style=\"fixed-case\">GCK<\/jats:styled-content> expression by <jats:styled-content style=\"fixed-case\">HFD<\/jats:styled-content>. Citral therapeutic effects were reconfirmed in diabetic rats. <jats:italic>In vitro<\/jats:italic> data indicated that retinaldehyde had the strongest <jats:styled-content style=\"fixed-case\">PCK<\/jats:styled-content>1 induction in primary hepatocytes of diabetic rats compared with <jats:styled-content style=\"fixed-case\">HFD<\/jats:styled-content> rats and control rats, in line with the increased <jats:styled-content style=\"fixed-case\">RALDH<\/jats:styled-content>1 expression. Citral reversed the retinaldehyde\u2010induced <jats:styled-content style=\"fixed-case\">PCK<\/jats:styled-content>1 expression in primary rat hepatocytes and HepG2 cells. In conclusion, <jats:styled-content style=\"fixed-case\">RALDH<\/jats:styled-content>1 induction impaired glucose metabolism partly via modulating <jats:styled-content style=\"fixed-case\">PCK<\/jats:styled-content>1 and <jats:styled-content style=\"fixed-case\">GCK<\/jats:styled-content> expressions. Citral improved glucose metabolism through inhibiting <jats:styled-content style=\"fixed-case\">RALDH<\/jats:styled-content> activity.<\/jats:p>","DOI":"10.1111\/bcpt.13039","type":"journal-article","created":{"date-parts":[[2018,5,12]],"date-time":"2018-05-12T23:00:11Z","timestamp":1526166011000},"page":"539-548","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Contribution of Hepatic Retinaldehyde Dehydrogenase Induction to Impairment of Glucose Metabolism by High\u2010Fat\u2010Diet Feeding in C57<scp>BL<\/scp>\/6J Mice"],"prefix":"10.1111","volume":"123","author":[{"given":"Jiong","family":"Xu","sequence":"first","affiliation":[{"name":"Center of Drug Metabolism and Pharmacokinetics School of Pharmacy China Pharmaceutical University Nanjing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mian","family":"Zhang","sequence":"additional","affiliation":[{"name":"Center of Drug Metabolism and Pharmacokinetics School of Pharmacy China Pharmaceutical University Nanjing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiangping","family":"Zhang","sequence":"additional","affiliation":[{"name":"Center of Drug Metabolism and Pharmacokinetics School of Pharmacy China Pharmaceutical University Nanjing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hanyu","family":"Yang","sequence":"additional","affiliation":[{"name":"Center of Drug Metabolism and Pharmacokinetics School of Pharmacy China Pharmaceutical University Nanjing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Binbin","family":"Sun","sequence":"additional","affiliation":[{"name":"Center of Drug Metabolism and Pharmacokinetics School of Pharmacy China Pharmaceutical University Nanjing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhongjian","family":"Wang","sequence":"additional","affiliation":[{"name":"Center of Drug Metabolism and 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