Fig. 3: DOP inhibition activates insulin secretion from human beta cells and islets. | Nature Communications

Fig. 3: DOP inhibition activates insulin secretion from human beta cells and islets.

From: Functional genetics reveals the contribution of delta opioid receptor to type 2 diabetes and beta-cell function

Fig. 3: DOP inhibition activates insulin secretion from human beta cells and islets.The alternative text for this image may have been generated using AI.

(A) Insulin secretion was assessed in EndoCβH5 cells treated with no glucose (green; LG) either with 10 μM NTI (n = 10 independent cell preparations), 5 μM DII (n = 12), a combination of both (n = 12) or no treatment (n = 12), for 40 min. (B) Insulin secretion was assessed in EndoCβH5 cells treated with 20 mM glucose (violet; HG) supplemented with 10 μM NTI (n = 10), 5 μM DII (n = 12), a combination of both (n = 12) or no treatment (n = 11), for 40 min. (C) Insulin secretion was assessed in human islets treated with 2.8 mM glucose (green; LG) supplemented with 10 μM NTI (n = 24 single isolated islets), 5 μM DII (n = 24), a combination of both (n = 29), or no treatment (n = 28), for 120 min. (D) Insulin secretion was assessed in human islets treated with 16.7 mM glucose (violet; HG) supplemented with 10 μM NTI (n = 23), 5 μM DII (n = 24), a combination of both (n = 29) or no treatment (n = 28), for 120 min. Data are box plots (showing the minimum, the median, the maximum, as well as all data). P-values are shown relative to control by unpaired two-tailed Mann-Whitney test. DII, [D-Ala2]-Deltorphin II; HG, high glucose; LG, low glucose; ns, not significant; NTI, naltrindole.

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