ArticleMolecular metabolism2026
Molecular mechanisms of lipid sensing in human cholecystokinin-secreting enteroendocrine cells.
Article in Molecular metabolism, 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
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesCholecystokinin (CCK) has been implicated in coordinating lipid digestion and satiety. However, the molecular mechanisms underlying nutrient-dependent CCK-release from human I-cells are not well understood, at least in part due to the cells' scattered distribution and a lack of reliable CCK-assays. Here we used human intestinal organoids to characterize lipid-sensing mechanisms underlying CCK release.
methodsHuman duodenal organoids were genetically engineered using CRISPR-Cas9 to insert either the fluorescent protein Venus or the cAMP reporter Epac-S-H187 at the CCK locus. Transcriptomic profiling of CCK-positive and negative cells was performed following fluorescent-activated cell sorting. Intracellular calcium and cAMP as well as CCK-GRAB-sensor secretory responses were assessed during live-cell imaging, and CCK secretion was quantified by LC-MS/MS. To evaluate lipid-sensing pathways, FFAR1, FFAR4, and GPR119 knockout organoids were generated.
resultsTranscriptomic analysis identified expression of lipid-sensing GPCRs in I-cells, including FFAR1, FFAR4, FFAR2, GPR119, GPBAR1, OR51E1 and OR51E2. Fatty acids and FFAR1 agonists increased intracellular calcium, whereas agonists of GPBAR1 and GPR119, and short-chain fatty acids elevated cAMP. CCK release was triggered by FFAR1, GPBAR and GPR119 agonists, and fatty acids with chain-length > C
conclusionsIn human I-cells, FFAR1 plays a crucial role in lipid-induced CCK release, whereas FFAR4 appears to be redundant in this context. These findings improve understanding of human CCK physiology and identify potential therapeutic targets for metabolic regulation and appetite control.
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.