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. 2018 Nov 13;68(2):430–440. doi: 10.2337/db18-0845

Figure 7.

Figure 7

NLRP3 is responsible for bladder dysfunction associated with DBD. The results of various parameters measured through cystometry are shown for nondiabetic (non-diab) and diabetic (diab) mice that either express NLRP3 (NLRP3+/+) or have that gene deleted (NLRP3−/−). All studies were performed at 15 weeks of age, and animals were implanted with a suprapubic catheter 1 week prior to analysis. A: Voiding volume in nondiabetic and diabetic mice (both NLRP3+/+). B: Voiding volume in nondiabetic and diabetic mice with NLRP3 deleted (NLRP3−/−). C and D: Frequency of voiding in the indicated animals. E and F: The PVR volume, or volume of urine remaining in the bladder immediately after the last void, in the indicated animals. No PVR was ever detected in any of the nine nondiabetic/NLRP3+/+ mice examined. G and H: The voiding efficiency of the indicated animals calculated as 100 (voided volume)/(voided volume + PVR). For all graphs, bars are mean ± SEM. n = 9 and 7 for nondiabetic and diabetic mice, respectively, that are NLRP3+/+. N = 10 and 9 for nondiabetic and diabetic mice, respectively, that are NLRP3−/−. **P < 0.01; ***P < 0.001 by a Student two-tailed t test. ANOVA followed by Tukey post hoc test was also used to compare all groups for each end point. The only additional significant differences found were in void volume comparing NLRP3+/+ diabetic to NLRP3−/− diabetic (P < 0.05) and voiding efficiency comparing NLRP3+/+ diabetic to NLRP3−/− nondiabetic.