Fig. 2: Deletion of Osgep in islet β-cells accelerated body weight gain and impaired glucose homeostasis under the CD-fed condition.

a Body weight curve of male (WT n = 6, Osgep-Ins2-Cre n = 5) mice was monitored weekly till 40 weeks. b Fasting blood glucose of male WT (n = 7) and Osgep-Ins2-Cre (n = 5) mice were monitored in 5, 15, and 30-week-old. IPGTT (c–e) in male mice at 8 (WT n = 7, Osgep-Ins2-Cre n = 6), 12 (WT n = 6, Osgep-Ins2-Cre n = 5), and 36-week-old (WT n = 5, Osgep-Ins2-Cre n = 5). ITT (f–h) in male mice at 8 (WT n = 6, Osgep-Ins2-Cre n = 5), 12 (WT n = 6, Osgep-Ins2-Cre n = 5), and 36-week-old (WT n = 6, Osgep-Ins2-Cre n = 6). Fasting serum insulin levels (WT n = 7, Osgep-Ins2-Cre n = 5) i, j and in vivo GSIS (WT n = 6, Osgep-Ins2-Cre n = 5) k, l were monitored at 12, and 36-week-old. m Islets number count of male WT and Osgep-Ins2-Cre mice (n = 6). n The representative images of immunofluorescence staining (IF) for insulin (green), Glucagon (red), and nucleus (blue) in sections from male WT and Osgep-Ins2-Cre mice (n = 6 biological replicates), and the proportion of α-cells and β-cells in the total islet cells. a–n Data are presented as the mean ± SD. a, c–h, k, l One-way ANOVA with Tukey’s post-test and Unpaired two-tailed Student’s t-test. b, i, j, m, n Unpaired two-tailed Student’s t-test. *p < 0.05, ** p < 0.01; *** p < 0.001. Source data are provided as a Source Data file.