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. 2022 Apr 15;13(4):353. doi: 10.1038/s41419-022-04767-z

Fig. 5. Pharmacological activation of REV-ERBα attenuates β-cell secretory function.

Fig. 5

A Isolated human islets were exposed to REV-ERB agonist (SR9009, 20 μM, for either 24 h or 72 h) or control (DMSO). Following a 30 min quiescent period in Krebs 4 mM glucose (G4), islets were stimulated with 16 mM glucose (G16) for 30 min at 37 °C. The graph represents insulin secretion normalized to insulin content (n = 7–8 independent experiments). The bottom panel represents insulin content in human islets. Data are expressed as mean ± SEM; *P < 0.05, ***P < 0.001 vs. control. B INS-1E cells were exposed to REV-ERB agonist (SR9009, 5 or 10 μM, 24 h) or control (DMSO). Following a 2 h quiescent period in Krebs 1.4 mM glucose (G1.4), cells were stimulated with 16.7 mM glucose (G16.7) for 1 h at 37 °C; (G1.4 refers to non-stimulated cells). The graph represents insulin secretion normalized to insulin content (n = 4 independent experiments). The bottom panel represents insulin content in INS-1E cells. C INS-1E cells were exposed to REV-ERB agonist (SR9009, 5 or 10 μM, 24 h) or control (DMSO). mRNA expression of key β-cell identity and functional genes expressed as fold change relative to control expression (n = 4 independent experiments per condition). Data are expressed as mean ± SEM; ***P < 0.001, *P < 0.05 vs. control.