ArticleEndocrinology2026
Free fatty acid receptor 4 agonism stimulates insulin secretion via different mechanisms in mouse vs human islets.
Article in Endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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11 authors.
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Abstract
Activation of the free fatty acid receptor FFAR4 in pancreatic islets potentiates insulin and inhibits somatostatin (SST) secretion. Here, we investigated the relative roles of δ and β cells in the insulinotropic effect of FFAR4 activation in mouse and human islets. The effects of the FFAR4 agonists Compound A (Cpd A) and AZ13581827 on insulin and SST secretion were investigated in islets from mice following ablation of δ cells and deletion of SST and the G protein Gαz (Gnaz-/-), in purified mouse β and δ cells, in mouse β cell-only pseudo-islets, and in human islets and EndoC-βH5 cells. Ca++ dynamics were measured in δ cells from Gnaz-/- mouse islets and β cells from dissociated mouse islets and human islets. The insulinotropic effect of FFAR4 activation was lost in δ cell-ablated and SST-deficient mouse islets, purified mouse β cells, and β cell-only pseudo-islets. FFAR4 activation did not increase β-cell Ca++ transients in dissociated mouse islets. Gαz deletion in mice partially blunted Cpd A inhibition of SST secretion but not the potentiation of insulin release. Cpd A diminished Ca++ transients in mouse δ cells, an effect that was partially lost in Gαz deficient islets. In human islets, Cpd A increased insulin secretion and intracellular Ca++ without affecting SST secretion. AZ13581827 potentiated insulin secretion in human EndoC-βH5 cells. We conclude that FFAR4 activation stimulates insulin secretion from mouse islets indirectly, in part via Gαz-coupled inhibition of SST secretion from δ cells, while in human islets, it directly stimulates insulin release from β cells.
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