ArticleNature communications2026
Gα
Article in Nature communications, 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
17 authors.
Funding
Abstract
Maintenance of glucose and lipid homeostasis is essential for metabolic health, and its dysregulation, driven by complex gene-environment interactions-underlies various metabolic disorders. Free fatty acid receptor 4 (FFAR4) has been proposed to link dietary signals with genetic metabolic predisposition, yet the precise mechanisms underlying the pathophysiological function of FFAR4 remain elusive and lack of the highly selective FFAR4 agonists. Our study shed light on the pivotal role of FFAR4 in metabolic homeostasis within metabolic organs. Hepatic FFAR4 deficiency in mice exacerbates lipid accumulation and promoted severe steatosis, whereas its overexpression ameliorates diet-induced metabolic dysfunction. Mechanistically, suppression of hepatic FFAR4 promotes lipogenesis by enhancing co-activation of the nuclear receptor Nr1h3 and PPARγ. Furthermore, we identify bavachalcone, a non-carboxylated compound isolated from the traditional Chinese medicine Psoralea corylifolia L., as a functionally effective FFAR4 agonist, which could robustly attenuate metabolic dysfunction. Structural analysis using cryo-electron microscopy reveals the binding mode of bavachalcone within the FFAR4-Gα
Indexed as
Identifiers
What Socratic 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 Socratic graph.