Anti-Obesity Effects of Fatdizol, a Blend of and , in 3T3-L1 Cells and Obese Mouse Models.

This study explored the anti-obesity potential of Fatdizol, a blend composed of L. and , in differentiated 3T3-L1 adipocytes and in a high-fat diet (HFD)-induced obese mouse model. High-performance liquid chromatography analysis of Fatdizol verified the presence of two key bioactive constituents, rosmarinic acid and 1-deoxynojirimycin (1-DNJ), which are recognized for their anti-obesity effects. In vitro, the influence of Fatdizol on adipogenesis and lipogenesis was assessed through glycerol release assays, Oil Red O staining, and Western blotting. Fatdizol treatment notably reduced lipid accumulation and triglyceride content while enhancing glycerol release in differentiated adipocytes. In vivo, obesity was induced in C57BL/6J mice by administration of a 60% HFD, followed by oral supplementation with Fatdizol for 16 weeks. Various analyses, including micro-computed tomography imaging, enzyme-linked immunosorbent assay of plasma, adipose tissue, and feces, histological evaluation by hematoxylin and eosin staining of adipose tissues and liver, and western blot analysis, were conducted. Fatdizol administration significantly attenuated body weight gain, reduced white adipose tissue (WAT) and brown adipose tissue mass, improved serum lipid profiles, and decreased both systemic WAT accumulation and lipid droplet size. Mechanistically, Fatdizol inhibited adipogenic and lipogenic protein expression, enhanced lipolytic pathways, stimulated energy metabolism, activated the phosphatidylinositol 3-kinase/protein kinase B signaling axis, and promoted glucose metabolism. Collectively, these findings suggest that Fatdizol holds significant promise as a therapeutic agent for obesity management and may serve as a functional ingredient for health-promoting food development if its efficacy can be confirmed in human clinical trials.