Fig. 2: POMC is downregulated in the PNS of mice with experimental diabetes.

Measuring 12 weeks STZ-treated diabetic mice and age-matched controls (STZ-untreated) for: a mechanical hyperalgesia (control, n = 13 and diabetic, n = 18; two-way ANOVA followed by Sidak’s post-hoc test; ***p < 0.001). PWR = paw withdrawal responses and b thermal hyperalgesia (control, n = 11 and diabetic, n = 12; two-tailed t-test; ***p < 0.0001). PWL = paw withdrawal latency (circles). c Pomc gene expression (18srRNA normalized) quantified in lumbar DRG, sciatic nerves (SN), and footpads (n = 5–6 mice/group; two-way ANOVA followed by Sidak’s post-hoc test; ***p < 0.0001). d Typical examples of co-immunostainings showing POMC protein expression (Rb anti-POMC antibody) in Tuj-1+ neurons in the DRG of control and diabetic mice (n = 5 mice/group, 5–9 DRG sections from each mouse) e Representative blots showing comparison of POMC protein level (using Gt antibody) in total lysates of lumbar DRG, SN, and footpads (control, n = 9 and diabetic, n = 9) f ß-endorphin level in lumbar DRG, SN, and footpads of control and diabetic mice quantified by ELISA (n = 6 mice/group, 2 replicates from each mouse; two-way ANOVA followed by Sidak’s post-hoc test; **p = 0.0049, ***p < 0,0001). For all panels, female mice data are shown; data represent mean ± SEM; with 95% C.I. Circles represent mean value per mouse in panel (b) and individual data points in panels (c, f). For panel (a), solid line with circles represents control mice and dotted line with black squares represents diabetic mice. For panel (c), white bar: control and orange bar: diabetic mice. Scale = 20 μm. Source data are provided as a Source Data file.