Fig. 2: Septin5 KO mice have superior glucose tolerance as a result of higher biphasic GSIS.

a–d IPGTTs were performed to assess blood glucose (a, b) and secreted insulin levels (c, d) and shown as AUC (area under the curve) analysis encompassing 120 min of the IPGTT for blood glucose (b) and insulin levels (d). N = 5 mice for each group, with summary graphs shown as mean ± SEM. Septin5 deletion was first confirmed in isolated islets, which did not affect the total islet insulin content (Supplementary Fig. 2a). For boxplots, boxes indicate 25th and 75th percentiles, the lines within boxes mark medians, whiskers above and below boxes indicate the 90th and 10th percentiles. e Blood glucose levels during IPITT showing no significant difference (n = 4 for control, and 6 for Septin5 KO from three biologically independent experiments). f Total insulin content is not affected in Septin5 KO mice. g–h Biphasic GSIS determined by Islet perifusion assays (g) of WT vs Septin5 KO mice and the corresponding AUC analysis (h) for first phase (first 10 min) and second phase (next 20 min) GSIS. Summary graphs from 4 biologically independent experiments shown as mean ± SEM. i Insulin-immunostained pancreatic sections. Septin5 KO does not alter the size, number and distribution of islets within the pancreas. Supplementary Fig. 2b, c shows the analysis for islet size and number. Scale bars, left, 1 mm, right, 100 µm. Statistical significance was assessed by a two-tailed Student’s t-test (*p < 0.05, the precise statistical results indicated in figures). Source data are provided as a Source Data file.