Fig. 3: Deletion of Osgep in islet β-cells aggravated abnormal glucose metabolism under HFD-feed for 16 weeks.

Body weight gain (a), fasting blood glucose (b), IPGTT (c–e), and ITT (f) were conducted in HFD-fed mice (HFD-WT n = 6, HFD-Osgep-Ins2-Cre n = 5). g Protein of p-Akt and total Akt were detected in liver and WAT of HFD-feed mice. The protein samples derive from the same experiment and that blots were processed in parallel. In vivo GSIS (h) and fasting serum insulin levels (i) were conducted in HFD feeding mice (HFD-WT n = 6, HFD-Osgep-Ins2-Cre n = 5). In vitro GSIS assays (HFD-WT n = 4, HFD-Osgep-Ins2-Cre n = 4) (j), and islets number count (HFD-WT n = 6, HFD-Osgep-Ins2-Cre n = 8) (k) were performed in islets isolated from HFD-fed mice. l Hematoxylin and eosin (H&E) stain analysis of the pancreatic sections and quantification of islet area (HFD-WT n = 6, HFD-Osgep-Ins2-Cre n = 5). m Representative immunofluorescence staining (IF) images showing major islet hormones anti-insulin (red), anti-glucagon (green), and anti-DAPI (blue) in pancreatic sections from HFD-fed mice (n = 6), and the proportion of α-cells and β-cells in the total islet cells. n Electron microscopy analysis of mice islet, arrowheads denoted insulin granules (n = 6). a–f, h–m Data are presented as the mean ± SD. a, b, i–m Unpaired two-tailed Student’s t-test. c–f, h One-way ANOVA with Tukey’s post-test and Unpaired two-tailed Student’s t-test. *p < 0.05, **p < 0.01; ***p < 0.001; ****p < 0.0001. Source data are provided as a Source Data file. HFD High fat diet, WAT White adipose tissue.