ArticleFrontiers in cell and developmental biology2026
DPP4 inhibition affects metabolism and inflammation associated pathways in hiPSC-derived steatotic HLCs.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Metabolic dysfunction-associated steatotic liver disease (MAFLD) has a high prevalence and high comorbidity for other diseases. Due to the complexity of this multifactorial disease, therapy options are still rather limited. We employed an Methods: We induced the steatosis phenotype in human induced pluripotent stem cell (iPSC)-derived hepatocyte-like cells (HLCs) by oleic acid (OA) feeding and confirmed regulation of clinically relevant pathways by NGS-based global transcriptomic analyses. Analysis of the secretome of steatotic HLCs revealed DPP4 as a potential key mediator of the disease. To further elucidate its role in the development of MAFLD, we inhibited DPP4 activity with vildagliptin (VILDA) and analyzed the global transcriptomic changes and specific gene and protein gene expression of steatosis-associated genes with and without DPP4 inhibition. Results: MAFLD-associated pathways such as PPAR and TNF signaling were differentially regulated in hiPSC-derived steatotic HLCs. We found increased hepatic DPP4 activity and secretion upon OA feeding. Gene expression of fatty acid and purine metabolism and inflammation-associated pathways was regulated upon DPP4 inhibition. Discussion: Our HLC model confirmed the association of DPP4 with metabolism and inflammation, which foster the development of MAFLD. Inhibiting DPP4 activity with VILDA partially relieved the steatotic phenotype on a global transcriptomic level. Impact and implications: Given the difficulties of identifying suitable anti-MAFLD drugs, novel model systems are urgently needed. Our
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