- Functional dyspepsia involves gastric sensorimotor dysfunction, impaired duodenal barrier, low-grade immune activation and altered neuroimmune signalling.
- PPARs regulate epithelial differentiation, inflammatory responses, mitochondrial metabolism, redox balance and lipid-mediator signalling relevant to duodenal homeostasis.
- Plant-derived bioactives modulate PPAR-linked pathways and mucosal adaptation, but human evidence for restoring duodenal function or clinical benefit remains uncertain.
Phytother Res. 2026 Sep 13. doi: 10.1002/ptr.70449. Online ahead of print.
ABSTRACT
Functional dyspepsia (FD) is a common disorder of gut-brain interaction in which gastric sensorimotor abnormalities may coexist with impaired duodenal barrier function, low-grade immune activation, and altered neuroimmune signaling. Peroxisome proliferator-activated receptors (PPARs) are relevant to this emerging model because they regulate epithelial differentiation, inflammatory responses, mitochondrial metabolism, redox balance, and lipid-mediator signaling. Impaired duodenal release of palmitoylethanolamide (PEA) provides direct translational evidence that defective PPARα-dependent lipid signaling may contribute to FD. Experimental studies further suggest that several plant-derived bioactives modulate PPAR-related pathways and other mechanisms involved in mucosal adaptation. Whether these effects restore duodenal function or improve clinically meaningful outcomes in humans remains uncertain. This review examines PPAR signaling as a mechanistic link between duodenal dysfunction and the actions of plant-derived bioactives. Therefore, we distinguish disease-specific evidence from findings obtained in other experimental settings and identify priorities for the development of mechanism-based phytotherapy in FD.
PMID:42732972 | DOI:10.1002/ptr.70449
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