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Image Search Results


Primary cilia are required for GLP-1-potentiated insulin secretion. ( A ) Dynamic insulin secretion from perifused mouse islets. Wild-type (WT, black) and β-cell-specific cilia knockout (βCKO, red) islets were sequentially exposed to 2 mM glucose (2G), 16 mM glucose (16G), 20 nM liraglutide (Lira), and 30 mM KCl as indicated. n = 6 replicates of 50 islets per genotype from 5 mice. ∗p < 0.05, two-way ANOVA with Sidak's multiple comparisons test. ( B ) Quantitative analysis of secretion traces: area under the curve (AUC) during initial glucose stimulation (minutes 10–30), liraglutide stimulation (minutes 30–50), KCl depolarization (minutes 60–70), and total AUC of the entire perifusion (minutes 0–70). βCKO islets secreted significantly less insulin in response to glucose and liraglutide but showed no defect in KCl-induced secretion. Data are mean ± SEM. ∗∗p < 0.01; ns, not significant, unpaired student's t-test. ( C-D ) IFT88 knockdown impairs GLP-1-augmented secretion in human islets. Static glucose-stimulated insulin secretion (GSIS) assays from islets of three male ( C ) and three female ( D ) donors. Islets transduced with control (Ctl, white) or IFT88 -targeting shRNA (IFT88 KD, red) were incubated at 1 mM glucose (1G), 11 mM glucose (11G), and 11G + 100 nM liraglutide (Lira). Donor ages are indicated. IFT88 KD significantly reduced liraglutide-potentiated insulin secretion. Data are mean ± SEM of triplicate samples per donor. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001; ns, not significant; one-way ANOVA with Tukey's multiple comparisons test.

Journal: Molecular Metabolism

Article Title: Primary cilia regulate GLP-1 signaling in pancreatic β cells

doi: 10.1016/j.molmet.2026.102357

Figure Lengend Snippet: Primary cilia are required for GLP-1-potentiated insulin secretion. ( A ) Dynamic insulin secretion from perifused mouse islets. Wild-type (WT, black) and β-cell-specific cilia knockout (βCKO, red) islets were sequentially exposed to 2 mM glucose (2G), 16 mM glucose (16G), 20 nM liraglutide (Lira), and 30 mM KCl as indicated. n = 6 replicates of 50 islets per genotype from 5 mice. ∗p < 0.05, two-way ANOVA with Sidak's multiple comparisons test. ( B ) Quantitative analysis of secretion traces: area under the curve (AUC) during initial glucose stimulation (minutes 10–30), liraglutide stimulation (minutes 30–50), KCl depolarization (minutes 60–70), and total AUC of the entire perifusion (minutes 0–70). βCKO islets secreted significantly less insulin in response to glucose and liraglutide but showed no defect in KCl-induced secretion. Data are mean ± SEM. ∗∗p < 0.01; ns, not significant, unpaired student's t-test. ( C-D ) IFT88 knockdown impairs GLP-1-augmented secretion in human islets. Static glucose-stimulated insulin secretion (GSIS) assays from islets of three male ( C ) and three female ( D ) donors. Islets transduced with control (Ctl, white) or IFT88 -targeting shRNA (IFT88 KD, red) were incubated at 1 mM glucose (1G), 11 mM glucose (11G), and 11G + 100 nM liraglutide (Lira). Donor ages are indicated. IFT88 KD significantly reduced liraglutide-potentiated insulin secretion. Data are mean ± SEM of triplicate samples per donor. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001; ns, not significant; one-way ANOVA with Tukey's multiple comparisons test.

Article Snippet: IFT88 knockdown in human islets: Healthy non-diabetic human islets were transduced with adenoviral vectors encoding either GFP-tagged shRNA targeting human IFT88 (Ad-GFP-h-IFT88-shRNA) or scrambled control (Ad-GFP-U6-scrmb-shRNA, #1122N; Vector Biolabs).

Techniques: Knock-Out, Knockdown, Transduction, Control, shRNA, Incubation