The absence of functional ASK1 does not ameliorate diabetes-associated sensory loss or nerve conduction velocity deficits.

<p>(A) Withdrawal responses to hindpaw mechanical stimulation (a 2 g Von Frey filament) touched to the hindpaw show that ASK1n mice develop sensory hypoalgesia in diabetes, similar to C57 mice. (B) The mean time taken for withdrawal of hindpaws from an infrared heat source is increased as a result of diabetes. There was exacerbation of this thermal hypoalgesia in one cohort of diabetic ASK1n mice, but was not repeated in two subsequent trials (one shown in C; NS not significant; **p<0.01; ***p<0.001 in a 2-way ANOVA on area under curve, with Bonferroni <i>post hoc</i> tests. Mean values ± SEM are displayed (<i>n</i> = 9–13)). (D) Motor nerve conduction velocities (MNCV) deficits were measured in both C57 and ASK1n mice from 8 weeks of diabetes compared with controls; p<0.001 at 8 weeks and p<0.05 at 12 weeks overall in a 2-way ANOVA, **p<0.01, ***p<0.001 in Bonferroni <i>post hoc</i> tests (<i>n</i> = 9–11). Note, there were no significant differences in near-nerve temperature in any group apart from the 8-week C57 cohort (control 33.9±0.6°C, diabetic 33.0±0.9°C, p<0.05; 2-way ANOVA, with Bonferroni <i>post hoc test</i>).