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The blood samples of 294 Chinese Han patients with type 1 diabetes mellitus(T1DM) and 199 controls were collected and their genomic DNAs were extracted. The single nucleotide polymorphisms rs17534481, rs12095738, rs2988276, and rs6668182 of CD247 gene were detected. The results showed that rs17534481 polymorphism of CD247 gene was associated with T1DM in Chinese Han population, and T allele was a protective factor for type 1 diabetes mellitus( OR=0.667, P=0.037). There was no significant difference in genotype frequency and allele frequency of rs12095738, rs2988276, and rs6668182 between type 1 diabetes group and control group( P>0.05).
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Objective To explore the effect of walking on residual beta cell function and glycemic control in patients with type 1 diabetes mellitus.Methods A total of 117 type 1 diabetes mellitus patients who usually walked less than 5000 steps per day were given health education about exercise and divided into three groups according to their self-estimates of the number of walking steps they had taken daily in the previous 4 months:an absent exercise group (＜ 5000 steps/day),a basic exercise group (5000-10000 steps/day) and an active exercise group (＞ 10000 steps/day).Among them,34 were in absent group (23.5％ for males),45 were in basis exercise group (40.0％ for males) and 38 were in active exercise group (52.6％ for males).Fasting C-peptide,postprandial C-peptide,and postprandial C-peptide to glucose ratio were used to evaluate the residual beta cell function,while glycated hemoglobin A1c (HbA1c) and insulin dose-adjusted HbAlc (IDAAlc) were used to evaluate their glycemic control.Results The beta cell function and glycemic control showed a tendency to improve with increases in the number of walking steps.Fasting C-peptide,postprandial Cpeptide and the postprandial C-peptide to glucose ratio also increased significantly,while HbA1c and IDAA1c decreased significantly.After balancing the initial difference in the analysis of covariance,significant differences were still found among the 3 groups in the subjects' beta cell function and glycemic control during the follow-up.Linear regression showed that a large number of steps independently predicted better beta cell function.Conclusions In patients with type 1 diabetes mellitus,walking exercise may be effective for improving residual beta cell function and glycemic control.
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Objective To investigate the mechanism of interleukin-1β(IL-1β) mediating the vascular calcium desensitization of septic rats by down-regulating Rho kinase activity.Methods Thirty-two SD rats were randomly divided into the sham operation group,cecal ligation and puncture (CLP) 3 h group,CLP 6 h group and CLP 12 h group,8 cases in each group.The septic rat was duplicated by CLP.Then the plasma IL-1β level and calcium sensitivity of superior mesenteric arteries (SMAs) were detected at different time points.Their correlation was analyzed.VSMCc derived from SMAs were cultured and incubated with different concentrations of human recombinant IL-1β for 24 h.Then the influences of IL-1β on the MLC20 phosphorylation level,Rho kinase activity,G protein expression level and RhoGEF activity were observed.Results The calcium sensitivity of SMAs after CLP 3 h began to decrease(P＜0.05),while plasma IL-1β level began to increase after CLP 6 h (P＜0.05),the change trend of SMAs calcium sensitivity was negatively correlated with plasma IL-1β level change(P＜0.05).IL-1β could decrease the phosphorylation level of VSMCs myosin light chain(MLC20) and Rho kinase activity(P＜0.05),up-regulate Gα11 expression and down-regulate Gα12 expression,but had no obvious effect on Gαq and Gα13 expression(P＞0.05).IL-1β could significantly reduce RhoGEF and PDZ-RhoGEF activity(P＜0.05) but significantly increase p63 Rho GEF activity(P＜0.05).Conclusion IL-1β induces the decrease of PDZ-RhoGEF and Rho kinase activity by down-regulating Gα12 expression,causes the decrease of MLC20 phosphorylation level,thus mediates the occurrence of calcium desensitization in septic rat;in addition,IL-1β may cause the increase of p63 RhoGEF activity by upregulating Gα11 expression,thus mediates the increase of vascular calcium sensitivity in septic rats,but the total effect is the decrease of calcium sensitivity.
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Objective To investigate the mechanism of interleukin-1β(IL-1β) mediating the vascular calcium desensitization of septic rats by down-regulating Rho kinase activity.Methods Thirty-two SD rats were randomly divided into the sham operation group,cecal ligation and puncture (CLP) 3 h group,CLP 6 h group and CLP 12 h group,8 cases in each group.The septic rat was duplicated by CLP.Then the plasma IL-1β level and calcium sensitivity of superior mesenteric arteries (SMAs) were detected at different time points.Their correlation was analyzed.VSMCc derived from SMAs were cultured and incubated with different concentrations of human recombinant IL-1β for 24 h.Then the influences of IL-1β on the MLC20 phosphorylation level,Rho kinase activity,G protein expression level and RhoGEF activity were observed.Results The calcium sensitivity of SMAs after CLP 3 h began to decrease(P＜0.05),while plasma IL-1β level began to increase after CLP 6 h (P＜0.05),the change trend of SMAs calcium sensitivity was negatively correlated with plasma IL-1β level change(P＜0.05).IL-1β could decrease the phosphorylation level of VSMCs myosin light chain(MLC20) and Rho kinase activity(P＜0.05),up-regulate Gα11 expression and down-regulate Gα12 expression,but had no obvious effect on Gαq and Gα13 expression(P＞0.05).IL-1β could significantly reduce RhoGEF and PDZ-RhoGEF activity(P＜0.05) but significantly increase p63 Rho GEF activity(P＜0.05).Conclusion IL-1β induces the decrease of PDZ-RhoGEF and Rho kinase activity by down-regulating Gα12 expression,causes the decrease of MLC20 phosphorylation level,thus mediates the occurrence of calcium desensitization in septic rat;in addition,IL-1β may cause the increase of p63 RhoGEF activity by upregulating Gα11 expression,thus mediates the increase of vascular calcium sensitivity in septic rats,but the total effect is the decrease of calcium sensitivity.
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The impact of glucagon on diabetes mellitus has become a hot area at present .Researchers hold that both the lack of isletβcells and islet αcells dysfunction exist in Type 1 diabetes mellitus (T1DM).Glucagon plays an important role in the occur-rence and development of T1DM, such as regulating the blood glucose and βcell function.Currently, a new therapy model represented by incretin is emerging , aiming at adjusting islet αcells function.And it has the prospect of becoming a new treatment of T 1DM be-sides insulin.Here we summarize the effect of glucagon on blood glucose and βcell function in T1DM, as well as the progress of T1DM treatment with glucagon as the therapeutic target .