ArticleChemistry & biodiversity2026
Network Pharmacology-Based Study of Citrus medica L. Ethanol Extract Combating Obesity in Caenorhabditis elegans via Dual Action on AAK-2/NHR-49 and MDT-15/SBP-1 Pathways.
Article in Chemistry & biodiversity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity, a complex metabolic disease, is tightly linked to lipid metabolism disorders. Jinhua Citrus medica Ethanol Extract (CMEE), a substance derived from a food-medicinal source, exhibits significant lipid-lowering and antioxidant properties; however, its systematic mechanisms of action remain incompletely elucidated. This study explored CMEE's anti-obesity and antioxidant mechanisms using a high-glucose-induced Caenorhabditis elegans (C. elegans) model. Network pharmacology predicted that the key mechanisms of CMEE involved the AMPK and PPAR signaling pathway. CMEE treatment notably reduced lipid accumulation levels, extended C. elegans lifespan, and enhanced antioxidant capacity. Mechanistically, CMEE was found to concertedly regulate lipid homeostasis through dual pathways. It activated the AMPK pathway (via aak-2) and upregulated the nuclear receptor NHR-49, thereby promoting the expression of key β-oxidation genes (acs-2, ech-1.1, cpt-1, cpt-2) to enhance fatty acid breakdown. Concurrently, it inhibited the MDT-15/SBP-1 pathway, downregulating desaturase genes (fat-5, fat-6, fat-7) to suppress fat synthesis. Combining network pharmacology, transgenic C. elegans fluorescence assays, and key gene mutant validation, this study established a complete evidence chain from prediction to verification. It clarified CMEE's multi-target role in ameliorating obesity and related metabolic disorders, providing theoretical and experimental support for its development as a functional food.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.