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

Fig. 8. Negative modulation of REV-ERBα partially protects from glucotoxicity-induced β-cell dysfunction.

Fig. 8

A INS-1E cells were exposed to glucotoxicity [30 mM glucose (G30) vs. control 11 mM glucose (G11)] for 48 h in the presence or absence of REV-ERB antagonist (SR8279, 10 μM). 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 DNA concentration (n = 4 independent experiments). B REV-ERBα was silenced in INS-1E cells by siRNA. Scramble RNA (Scr) was used as a control. Cells were then exposed to glucotoxicity for 48 h (G30 vs. G11). 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 DNA concentration (n = 4 independent experiments). The bottom graphs represent the stimulation index (ratio G16.7: G1.4). Data are expressed as mean ± SEM; *P < 0.05, **P < 0.01, ***P < 0.001 vs. G1.4 (unless specified).