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. 2015 Oct 5;65(1):53–61. doi: 10.2337/db15-0770

Figure 1.

Figure 1

miR-29a prevents diabetes during unfolded protein stress by positive regulation of insulin secretion. A–D: Unmanipulated wild-type, miR-29a+/−, and miR-29a−/− mice, as well as miR-29a−/− mice transplanted with wild-type islets, were fasted for 6 h. Fasting blood glucose levels (n = 19, 20, 19, and 5, respectively) (A) and fasting serum insulin levels (n = 16, 15, 9, and 6) (B). Blood glucose levels (n = 19, 20, 19, and 5) (C) and serum insulin levels (n = 16, 15, 9, and 6) (D) after glucose challenge. E–H: Wild-type, miR-29c+/−, and miR-29c−/− mice were fasted for 6 h. Fasting blood glucose levels (n = 9, 13, and 7) (E) and serum insulin levels (n = 9, 13, and 7) (F). Blood glucose levels (n = 9, 13, and 7) (G) and serum insulin levels (n = 9, 13, and 7) (H) after glucose challenge. I: Representative histograms and mean fluorescence intensity (MFI) of anti-insulin antibody staining on islets purified from wild-type and miR-29a−/− mice (n = 5 and 4). J: Representative immunofluorescence staining on the pancreas of wild-type and miR-29a−/− mice for insulin (red) and glucagon (green) (n = 3 and 4). Scale bar indicates 50 μm. K: Whole pancreas was taken from wild-type and miR-29a−/− mice, and quantitative PCR was performed for insulin relative to Rpl37a. L–O: Islets were purified from wild-type and miR-29a−/− mice, and quantitative PCR was performed for insulin (L), Mct1 (M), Stx1a (N), and Vamp3 (O) relative to Rpl37a (n = 7,4). P: Diabetes incidence of insHEL transgenic males on the miR-29awt/wt (n = 11), miR-29awt/0 (n = 9), and miR-29a0/0 (n = 7) backgrounds. No diabetes was observed in mice of any genotype without the insHEL transgene. Median ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001. Het, heterozygote; KO, knockout; WT, wild-type.