Fig. 3: Impaired metabolic coupling of insulin secretion.

a The number of differentially expressed genes within the three groups (n = 3–4). b Gene expression profiles regulated by Raptor were subjected to hierarchical clustering (n = 3–4). c GO analysis of differentially expressed genes as identified by RNA-seq of 8-week-old WT (n = 3) and euglycemic βRapKO^GFP β-cells (n = 4) was associated with β-cell function. d Visualization of differential expression of genes involved in insulin secretion. e–g Relative expression of selected transcripts associated with β-cell secretion function (n = 5 independent sample for WT, n = 5 independent sample for diabetic βRapKO^GFP, n = 4 independent sample for euglycemic βRapKO^GFP, p values included in source data) (e), mitochondrial metabolism (n = 5 independent sample for WT, n = 5 independent sample for diabetic βRapKO^GFP, n = 4 independent sample for euglycemic βRapKO^GFP, p values included in source data) (f), and disallowed genes (n = 5 independent sample for WT, n = 5 independent sample for diabetic βRapKO^GFP, n = 4 independent sample for euglycemic βRapKO^GFP, p values included in source data) (g) in WT, diabetic βRapKO^GFP, and euglycemic βRapKO^GFP β-cells by qRT-PCR. h Representative immunofluorescent staining for Glut2 (red) and insulin (green) among 8-week-old WT, diabetic βRapKO^GFP, and euglycemic βRapKO^GFP mice (n = 3). Insets showed different expression levels of Glut2. Quantification of Glut2 areas in Ins⁺ areas in WT, diabetic βRapKO^GFP, and euglycemic βRapKO^GFP mice (n = 3, WT vs diabetic βRapKO^GFP: p = 0.002; diabetic βRapKO^GFP vs euglycemic βRapKO^GFP: p = 0.613; WT vs euglycemic βRapKO^GFP: p = 0.001), at least 10 islets from three sections were used for quantifications of Glut2. Scale bars, 20 μm. Data represent means ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001 by one-way ANOVA.