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. 2015 Jul 16;5:12144. doi: 10.1038/srep12144

Figure 8. UA leads to dyslipidemia and glucose intolerance mediated by NF-κB.

Figure 8

(A–C) Time course of serum biochemical parameters after the onset of HUAD feeding (n = 6 rats per group). (D–F) Serum biochemical parameters of the rats that were icv administered saline or UA for 1 and 2 weeks (n = 6 rats per group). (G–I) Blood pressure measurements (G) and an OGTT were performed in rats fed chow or a HUAD for 1, 2, and 3 months; glucose concentrations are plotted versus time (H) and as AUC (I, per 120 min) (n = 6 rats per group). (J) Quantification of fasting serum insulin concentration in rats fed chow or a HUAD for 1, 2, and 3 months (n = 6 rats per group). (K,L) An OGTT was performed in the rats that received icv administration of saline or UA (3000 ng/ml, 1 μl/min, 10 μl) for 1 and 2 weeks (icv-1w and icv-2w). The test was performed 24 h after the last dose of UA, and glucose concentrations are plotted versus time (K) and as AUC (L, per 120 min) (n = 6 rats per group). (M–O) OGTTs were performed in mice with icv injection of normal saline (N.S.) or UA (600 ng/ml or 3000 ng/ml, 1 μl/min, 2 μl), with (N) or without (M) icv injection of BAY11-7085 (250 mM, 1 μl/min, 2 μl) 30 min prior to the icv UA administration for 14 consecutive days. The test was performed 8 h after the last dose of UA, and glucose concentrations are plotted versus time (M,N) and as AUC (O, per 120 min) (n = 6 mice per group). (P–R) Serum biochemical parameters of the mice that were icv administered saline or UA, with or without icv injection of BAY11-7085 (n = 6 mice per group). All displayed values are the mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001 versus control; #P < 0.05; ##P < 0.01 versus without BAY11-7085 administration.