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. 2014 Oct 16;9(2):661–673. doi: 10.1016/j.celrep.2014.09.030

Figure 3.

Figure 3

Glucose-Dependent Production of Cytosolic Glutamate and Increased Glutamate Contents in Insulin Granules by cAMP/PKA Signaling

(A) Effect of glucose on total cellular glutamate contents in the absence or presence of GLP-1 (10 nM) in MIN6-K8 cells (n = 3 for each point).

(B and C) Changes in contents of glutamate isotopomers (M to M+5) by glucose stimulation in the absence or presence of GLP-1 (10 nM) in whole cells (B) and cytosol (C) in MIN6-K8 cells (n = 4–5 for each).

(D–F) Effects of AOA on contents of glutamate isotopomers (M+2 to M+5) in whole cells (D), cytosol (E), and mitochondria (F) in MIN6-K8 cells (n = 3 for each).

(G) Effects of glucose, GLP-1 (10 nM), H-89 (10 μM, a PKA inhibitor), and 8-pCPT (10 μM, 8-pCPT-2′-O-Me-cAMP-AM, an Epac-selective cAMP analog) on glutamate contents in insulin granules in MIN6-K8 cells (n = 4–12).

(H) Dose-dependent effects of GLP-1 on glutamate contents in insulin granules in MIN6-K8 cells under the glucose (11.1 mM)-stimulated condition (n = 4 for each).

The data are expressed as means ± SEM. Results are representative of three independent experiments. The Tukey-Kramer method was used for evaluation of statistical significance. ∗p < 0.05; ∗∗p < 0.01; n.s., not significant. See also Table S2 and Figure S3.