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We herein investigated the effects of calcium\/calmodulin\u2010dependent protein kinase II (CaMKII) inhibitors on diet\u2010induced obesity in mice. In mice fed a high\u2010fat diet (HFD), the administration of the CaMKII inhibitor KN\u201093 and the glycolipid acremomannolipin A with the suppression of CaMKII phosphorylation reduced fat mass in the whole body, epididymal and subcutaneous white adipose tissue weights, and lipid accumulation in epididymal and subcutaneous white adipose tissues, but not muscle mass or bone mineral density at the tibia. Moreover, the administration of KN\u201093 and acremomannolipin A improved glucose intolerance in HFD\u2010fed mice. In an in vitro study on preadipocytic 3T3\u2010L1 cells and mouse adipose tissue\u2010derived stromal cells, KN\u201093 and acremomannolipin A suppressed adipogenic differentiation, proliferation, and lipid accumulation. In conclusion, this is the first study to demonstrate that CaMKII inhibitors mitigated the development of diet\u2010induced obesity in mice partly through the suppression of adipogenic differentiation, cell proliferation, and lipid accumulation in adipocytes. Inhibiting CaMKII could be a potential strategy for obesity treatment.<\/jats:p>","DOI":"10.1155\/jobe\/5530467","type":"journal-article","created":{"date-parts":[[2025,6,30]],"date-time":"2025-06-30T12:18:49Z","timestamp":1751285929000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Calcium\/Calmodulin\u2010Dependent Protein Kinase II Inhibitors Mitigate High\u2010Fat Diet\u2013Induced Obesity in 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