Nrf2 Activation Protects Mouse Beta Cells from Glucolipotoxicity by Restoring Mitochondrial Function and Physiological Redox Balance

Figure 3

At physiological conditions, activation of Nrf2 inhibits insulin secretion and changes the glucose-dependent fast alterations in cellular ROS. (a, b) Murine islets were cultured in standard medium in the absence (white bars) or presence (grey bars) of oltipraz (10 μmol/L) or DMF (50 μmol/L) for 48 h. Thereafter, islets were stimulated with 3 or 15 mmol/L glucose for 1 h and insulin release was measured. (c–e) The same procedure as described for (a, b) but with dispersed islet cells. Acute 1 h stimulation with 15 mmol/L glucose did not reduce DHE-sensitive ROS compared to 0.5 mmol/L glucose (c) but still elevated DCF and BES-H₂O₂ fluorescence (d, e). Numbers in bars indicate the number of independent preparations (a, b) or cells (c–e). and ; n. s.: not significant.

(a)

(b)

(c)

(d)

(e)