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The <jats:italic>4\u2010O\u2010methylhonokiol<\/jats:italic> (MH) has been isolated mainly from the bark of the root and stem of Magnolia species. In this study, we aimed to elucidate whether MH can effectively prevent DCM in type 2 diabetic (T2D) mice and, if so, whether the protective response of MH is associated with its activation of AMPK\u2010mediated inhibition of lipid accumulation and inflammation. A total number of 40 mice were divided into four groups: Ctrl, Ctrl\u00a0+\u00a0MH, T2D, T2D\u00a0+\u00a0MH. Five mice from each group were sacrificed after 3\u2010month MH treatment. The remaining animals in each group were kept for additional 3 months without further MH treatment. In T2D mice, the typical DCM symptoms were induced as expected, reflected by decreased ejection fraction and lipotoxic effects inducing lipid accumulation, oxidative stress, inflammatory reactions, and final fibrosis. However, these typical DCM changes were significantly prevented by the MH treatment immediately or 3 months after the 3\u2010month MH treatment, suggesting MH\u2010induced cardiac protection from T2D had a memory effect. Mechanistically, MH cardiac protection from DCM may be associated with its lipid metabolism improvement by the activation of AMPK\/CPT1\u2010mediated fatty acid oxidation. In addition, the MH treatment of DCM mice significantly improved their insulin resistance levels by activation of GSK\u20103\u03b2. These results indicate that the treatment of T2D with MH effectively prevents DCM probably <jats:italic>via<\/jats:italic> AMPK\u2010dependent improvement of the lipid metabolism.<\/jats:p>","DOI":"10.1111\/jcmm.14493","type":"journal-article","created":{"date-parts":[[2019,6,14]],"date-time":"2019-06-14T12:10:51Z","timestamp":1560514251000},"page":"5771-5781","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["4\u2010O\u2010methylhonokiol protects against diabetic cardiomyopathy in type 2 diabetic mice by activation of AMPK\u2010mediated cardiac lipid metabolism improvement"],"prefix":"10.1111","volume":"23","author":[{"given":"Zongyu","family":"Zheng","sequence":"first","affiliation":[{"name":"Departments of Urology and Cardiology The First Hospital of Jilin University Changchun China"},{"name":"Department of Pediatrics Pediatric Research Institute, University of Louisville Louisville Kentucky"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tianjiao","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Pediatric Research Institute, University of Louisville Louisville Kentucky"},{"name":"Department of Rheumatology and Immunology China\u2010Japan Union Hospital of Jilin University Changchun China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hua","family":"Guo","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Pediatric Research Institute, University of Louisville Louisville Kentucky"},{"name":"Department of Immunology, Zhejiang Key Laboratory of Pathophysiology Medical School of Ningbo University Ningbo China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ki Soo","family":"Kim","sequence":"additional","affiliation":[{"name":"SK Bioland Haimen Co. 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