All of 143 patients with gout or hyperuricemia were divided into type 2 diabetes(n=43), impaired glucose regulation(n=45),and normal glucose tolerance(n=55)groups. Moreover,a cut point of 8.6 mmol/L in one hour postload plasma glucose(1hPG)of oral glucose tolerance test was used to sub-divide the normal glucose tolerance group into 1hPG≥8.6 mmol/L(n=30)and 1hPG<8.6 mmol/L(n=25)groups. The first-and second-phase insulin secretion indexes were compared among four groups. The results showed that there was no statistical difference in the second-phase insulin secretion index among impaired glucose regulation,1hPG≥8.6 mmol/L,and 1hPG<8.6 mmol/L groups(P>0.05). The first-phase insulin secretion index revealed no significant difference between impaired glucose regulation and 1hPG≥8.6 mmol/L groups(P>0.05),but obviously decreased in these two groups compared with 1hPG<8.6 mmol/L group(P<0.05). The modified β cell function indexes were gradually decreased in 1hPG<8.6 mmol/L,1hPG≥8.6 mmol/L, and impaired glucose regulation groups(P<0.05). These results suggest that when 1hPG of the patients with gout and hyperuricemia is over 8.6 mmol/L,the first-phase insulin secretion will be impaired.

This study was designed to explore the correlation between alterations in NLRP3 levels and Th17/Treg imbalance in asthmatic mice undergoing epithelial-mesenchymal transition(EMT).A murine model of asthma was established by intraperitoneal injection combined with nebulization of ovalbumin(OVA).Mice were randomly grouped into asthma model group and normal control group.The airway reactivity was detected with non-invasive lung function instrument.Hematoxylin and Eosin(HE)and Masson's trichrome staining were applied to evaluate the histopathological injury of lung tissue and the extent of lung fibrosis;RT-qPCR was applied to detect EMT-related biomarkers(Snail,E-Cadherin,N-Cadherin),the specific transcription factors of T cell subsets(RoRγt,Foxp3)and NLRP3 in lung tissue of mice;Western blot was used to detect the protein expression of E-cadherin,N-Cadherin and NLRP3 in lung tissue of mice.The Th17 and Treg cell populations in the spleen were enumerated via flow cytometry.Furthermore,the expression levels of NLRP3,IL-17 and IL-10 in bronchoalveolar lavage fluid(BALF)were analyzed by Giemsa staining.Compared with the control group,the asthma model group showed higher level of airway resistance,coupled with an obviously decrease in pulmonary ventilation compliance.Pathological alterations in lung tissue were evident,characterized by thickening of the airway epithelium,airway stenosis,infiltration of inflammatory cells,higher expression levels of N-Cadherin and NLRP3 proteins(P<0.05),lower expression level of E-Cadherin(P<0.001)and higher levels of marker genes(Snail and N-Cadherin)in lung tissue.Furthermore,model mice demonstrated higher level of NLRP3 in BALF(P<0.05),higher level of Th17 in spleen,and higher levels of retinoic acid orphan receptor(ROR)-γt mRNA(P<0.05)and Th17-related cytokines(IL-17)(P<0.01).Concurrently,model mice also showed an obviously decrease in the prevalence of Treg cells,Forkhead box Foxp3 mRNA(P<0.001),and Treg-related cytokine IL-10(P<0.05).The results of the Pearson correlation analysis indicated that the level of NLRP3 mRNA was positively correlated the ratio of RoR γt mRNA,but negatively correlated with Foxp3 mRNA in the lung tissue of asthmatic mice.Additionally,NLRP3 in BALF demonstrated a positive correlation with IL-17 and a negative correlation with IL-10.In conclusion,These findings suggest that NLRP3 may trigger bronchial EMT by exacerbating the immune imbalance of Th17/Treg cells.