Fig. 1: Serum CHGA in response to verapamil treatment of subjects with T1D.
CHGA as assessed by LC-MS/MS (y-axis represents relative abundance levels in zero-centered log2 form) in serum at baseline (BL) or at 1 year (Y1) of individual control subjects with T1D receiving placebo (black) (n = 5) (NS) (a) or verapamil (red) (n = 5) (t4 = 5.966, *P = 0.0040) (b). Comparison of the changes in CHGA (BL to Y1) as assessed by LC-MS/MS in the verapamil and the placebo group (t8 = 3.674, *P = 0.0063) (c). Serum CHGA levels at BL or Y1 as assessed by ELISA in individual control subjects with T1D receiving placebo (n = 6) (NS) (d) or verapamil (n = 9) (t8 = 5.44, *P = 0.0006) (e). Comparison of the changes in CHGA (BL to Y1) as assessed by ELISA in the verapamil and the placebo group (t13 = 4.497, *P = 0.0006) (f). Serum CHGA levels in healthy, non-diabetic volunteers (blue) (n = 9) as assessed by ELISA and compared to subjects with T1D at baseline (T1D BL) (white) (n = 15), subjects with T1D getting placebo for 1 year (Control T1D Y1) (n = 6) or receiving verapamil for 1 year (Verapamil T1D Y1) (n = 9) (F3,35 = 4.392, *P = 0.01) (g). Correlation of C-pep AUC and serum CHGA (R = −0.62, P = 0.0026) (h). Bars represent means ± SEM. For a, b, d, e, two-tailed, paired Student’s t-test. For c, f, two-tailed Student’s t-test. For g, one way ANOVA and for h, repeated measures correlation coefficient by mixed model. Subject characteristics are listed in Supplementary Table 1. Source data are provided as a Source Data file.
