Abstract
Background: Metabolic syndrome (MetS) is a global health concern, characterized by a combination of dyslipidemia, insulin resistance, obesity, and hypertension, significantly increasing the risk of type 2 diabetes mellitus (T2DM) and cardiovascular diseases. Gut microbiota plays a pivotal role in MetS pathophysiology, with dysbiosis exacerbating metabolic impairments. Delites™, a supplement inspired by Traditional Chinese Medicine, has shown potential in modulating gut microbiota and mitigating MetS. Objectives: This study aimed to evaluate the effects of Delites™ supplementation on metabolic health and gut microbiota composition in male Sprague Dawley rats fed a cholesterol- and fat-enriched diet (CFED). Methods: A randomized preclinical trial was conducted on 32 rats divided into four groups: control-normal, CFED, CFED+low-dose Delites™ (54 mg/kg), and CFED+high-dose Delites™ (108 mg/kg). Parameters including lipid profiles, enzymatic activity, molecular biomarkers, and gut microbiota composition were analyzed. Results: Delites™ significantly improved lipid profiles, reduced inflammation (TNF-α), enhanced anti-inflammatory markers (IL-10), and increased energy metabolism regulator PGC-1α. Gut microbiota modulation showed increased beneficial genera (Bifidobacterium, Lactobacillus) and reduced pathogenic Proteus, improving microbial diversity. Conclusion: Delites™ supplementation effectively mitigates MetS through metabolic and microbiota modulation. These findings highlight its potential for precision medicine approaches to combat metabolic disorders. Further research is needed to explore its long-term effects and translational relevance in humans.
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Leonardo, J., Hertanto, R., Surya, R., Syahputra, R. A., Humayrah, W., Sabrina, N., … Nurkolis, F. (2025). DelitesTM supplementation prevents metabolic syndrome onset and modulates gut microbiome in male Sprague Dawley rats fed on cholesterol- and fat-enriched diet: a randomized preclinical trial study. Frontiers in Nutrition, 12. https://doi.org/10.3389/fnut.2025.1571473
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