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Obesity / Anti Obesity Agents · Journal article
Pakistan Journal of Pharmaceutical Sciences
Early or partial results. Treat as a signal, not a conclusion.
This is a preclinical mouse study demonstrating that britanin, a sesquiterpene lactone, reduces weight and lipid markers in high-fat diet-induced obesity via MAPK pathway modulation identified through network pharmacology. The work is mechanistically sound but remains in animals with no human efficacy or safety data, and is insufficient to guide clinical practice.
Controlled animal experiment with mechanistic validation and network pharmacology analysis. C57BL/6J male mice; high-fat diet-induced obesity model; setting not specified. Intervention: Britanin (5 mg/kg and 15 mg/kg, intraperitoneal). Compared with: High-fat diet control (implied; specific comparator description not provided).
15 mg/kg britanin reduced body weight by 18% in high-fat diet mice Serum triglycerides decreased 45% (p<0.001), total cholesterol 37% (p<0.001), LDL-C 32% (p<0.01) Britanin reversed adipocyte hypertrophy and inhibited PPARγ-mediated adipogenesis
No human efficacy, pharmacokinetics, or safety data; species differences in MAPK regulation unknown
This study provides preclinical rationale for britanin as a potential anti-obesity agent but does not yet support human use. Progression to toxicology studies and clinical trials would be required before clinical translation.
Single-center animal study with mechanistic validation but no human data, uncontrolled design, and surrogate endpoints only; insufficient for clinical guidance despite sound experimental approach.
As stated by the source record.
Quoted from the source exactly as published.
This study provides preclinical rationale for britanin as a potential anti-obesity agent but does not yet support human use. Progression to toxicology studies and clinical trials would be required before clinical translation.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Background. The escalating prevalence of obesity has made it a critical public health concern. There is an urgent need to identify naturally derived compounds with anti-obesity potential. Britanin (BRI), a bioactive sesquiterpene lactone derived from Inula species, has shown promise in metabolic disorder management, but its anti-obesity mechanisms remain uncharacterized.Objectives. Combining animal experiments and network pharmacology analysis to explore the effect of BRI in high-fat diet-induced obesity.Methods. C57BL/6J male mice were used for experiment. A high-fat diet (HFD)-induced obese mouse model was treated with BRI (5/15 mg/kg, i.p.) to validate lipid metabolism and weight loss. Network pharmacology identified potential targets via SwissTargetPrediction, GeneCards and OMIM databases, with molecular docking (CB-DOCK) and PPI network analysis (STRING/Cytoscape). Relevant validations were conducted based on the screened targets. Additionally, a biosafety assessment was performed.Results. In-vivo, 15 mg/kg BRI reduced body weight by 18%, decreased serum TG (-45%, p<0.001), TC (-37%, p<0.001) and LDL-C (-32%, p<0.01) and reversed adipocyte hypertrophy. Thirty-nine intersection targets were identified, with MAPK1, EGFR, PTGS2, MAP2K1 and MAPK8 as top hubs (degree centrality >15). BRI exhibited strong binding affinity (-7.7 to -10.3 kcal/mol) to these targets. Mechanistically, BRI exerts its anti-obesity effects by regulating key targets within the MAPK signaling pathway, particularly MAPK1 and inhibited the PPARγ, thereby blocking adipogenesis and promoting the transition of adipose tissue.Conclusion. BRI may alleviate obesity by regulating the Mitogen-Activated Protein Kinase signaling pathway, providing a rationale for natural compound-based obesity therapy.
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