**Background:** Obesity is a global health crisis characterized by excess body fat due to chronic energy imbalance, leading to metabolic disorders such as type 2 diabetes, dyslipidemia, and fatty liver disease. White adipose tissue expands via hypertrophy and hyperplasia in response to overnutrition. Natural phenolic compounds from plants have emerged as potential anti-obesity agents with fewer side effects than conventional medications. Bainiku-ekisu (Prunus mume concentrate), black garlic, and Mesona procumbens Hemsl. (Hsian-tsao) have each shown independent metabolic benefits. This study developed a novel combination formula (Mei-Gin formula, MGF) and evaluated its anti-adipogenic and anti-obesity effects.
**Methods:** Seven MGF variants (MGF-1 through MGF-7) were prepared with different ratios of bainiku-ekisu, Prunus mume ethanol extract, black garlic water extract, and Hsian-tsao ethanol extract. Phenolic content was analyzed by HPLC. For in vitro experiments, 3T3-L1 preadipocytes were differentiated into mature adipocytes and treated with MGF-1-7 at concentrations of 0, 10, 25, 50, 100, and 250 μg/mL for 48 h. Lipid accumulation was assessed by Oil Red O staining and triglyceride quantification. GPDH activity was measured using a colorimetric assay kit. For in vivo experiments, 108 six-week-old male Wistar rats were divided into nine groups (n=12 each): normal diet (AIN-93G, 7% fat), high-fat diet (HFD, 32% lipids), HFD + low-dose Japan Mei-Gin (100 mg/kg), HFD + high-dose Japan Mei-Gin (300 mg/kg), HFD + low-dose MGF-3 (100 mg/kg), HFD + high-dose MGF-3 (300 mg/kg), HFD + low-dose MGF-7 (100 mg/kg), HFD + high-dose MGF-7 (300 mg/kg), and HFD + positive control (HCA + CGA, 140.6 mg/kg). Treatments were administered for 8 weeks. Body weight, feed intake, and water intake were measured throughout. After euthanasia, organs and adipose tissues (perirenal, epididymal, mesenteric, retroperitoneal, inguinal) were dissected and weighed.
**Key Results:** HPLC analysis showed MGF-7 had the highest chlorogenic acid content (0.72 mg/g), while MGF-4 had the highest caffeic acid content (0.26 mg/g). In 3T3-L1 adipocytes, all MGF variants reduced lipid accumulation and triglyceride levels in a dose-dependent manner. At 250 μg/mL, MGF-3 and MGF-7 reduced triglyceride content by 31.4% and 35.9%, respectively, compared to untreated controls. GPDH activity was decreased correspondingly, with MGF-3 and MGF-7 showing the greatest suppression. In the rat model, HFD rats had significantly higher final body weight (617 ± 16 g) compared to ND rats (512 ± 17 g). High-dose MGF-7 (300 mg/kg) reduced final body weight to 548 ± 18 g and weight change to 338 ± 18 g (vs. 406 ± 16 g for HFD, p < 0.05). Feed efficiency was significantly lower in the high-dose MGF-3 (31 ± 2%), high-dose MGF-7 (30 ± 2%), and positive control (30 ± 1%) groups compared to HFD (35 ± 1%). Liver weight was significantly reduced in low-dose JMG, high-dose MGF-3, both doses of MGF-7, and positive control groups. Total body fat was significantly lower in low-dose JMG (135 ± 5 mg/g), high-dose MGF-3 (132 ± 11 mg/g), low-dose MGF-7 (131 ± 7 mg/g), high-dose MGF-7 (126 ± 8 mg/g), and positive control (134 ± 8 mg/g) compared to HFD (168 ± 7 mg/g). Both visceral and subcutaneous adipose tissue depots were reduced, with significant decreases in perirenal and mesenteric adipose tissue. No significant differences were observed in heart, spleen, lung, or kidney weights across groups.
**Clinical Implications:** This study provides preclinical evidence that the Mei-Gin formula, particularly MGF-7, has significant anti-obesity effects by reducing adipocyte differentiation, lipid accumulation, and body fat deposition. The formula appears to act through suppression of GPDH activity, a key enzyme in triglyceride synthesis. The decompression processing method used may preserve more bioactive phenolic compounds compared to traditional thermal condensation. These findings support further investigation into MGF as a natural, plant-based therapeutic option for obesity management. However, the specific molecular mechanisms (e.g., lipolysis, fatty acid oxidation, thermogenesis pathways) remain to be elucidated, and human clinical trials are needed to establish efficacy and safety in humans.