Objective To observe the efficacy of rosiglitazone treatment in impaired glucose tolerance (IGT) with hyperinsulinemia. Methods 56 IGT patients were divided into two groups randomly:control group (28 cases) and rosiglitazone group (28 cases). Improving life style were given to control group,while improving life style and rosiglitazone (4mg/d) were given to rosiglitazone group for 12 weeks. The body mass index (BMI),fasting and postprandial plasma glucose,insulin and insulin sensitivity index (ISI) were observed. Results In control group the fasting and postprandial plasma glucose and insulin showed no difference between pre-and post-treatment (P>0.05).The levels of the fasting and postprandial plasma glucose and insulin dropped obviously in rosiglitazone group compared to both the baseline levels and the levels of control group at 12 weeks of treatment(P<0.05). The BMI and body weight dropped obviously in control group at 12 weeks of treatment (all P<0.05),but showed no difference in rosiglitazone group (P>0.05). The ISI increased markedly in rosiglitazone group (P<0.05),but showed no difference in control group (P>0.05). Conclusions The rosiglitazone treatment increases insulin sensitivity obviously,improves first-phase insulin secretion,and postpones the progression to T2DM from impaired glucose tolerance in patients with IGT

To compare the degree of glycemic excursions by dynamic glucose monitoring in type 2 diabetes in the elderly when their HbA_1c≤6. 5, The mean blood glucose level and hypoglycemia incidence were observed. The amplitude of glycemic excursions revealed by DGMS was significantly lower in insulin glargine group than in mixed insulin group (P<0.05). The incidence of hypoglycemia were lower in glargine group than in mixed insulin group(P<0.05).

Objective To investigate the effect of liraglutide and metformin hydrochioride on overweight diabetic patients because of poor glycemic control.Methods Forty-four overweight patients with poor glycemic control were randomly divided to the control group,the liraglutide group and the metformin hydrochioride group.Patients in control group were given diet and exercise control,in liraglutide group and the metformin hydrochioride group were given subcutaneous injection liraglutide,metformin hydrochioride oral treatment respectively for 12 weeks.Body mass index(BMI),fasting blood glucose (FBG),2-hour postprandial blood glucose (2 hPBG) and glycosylated hemoglobin (HbA1c) were measured.Results Compared with pretreatment,FBG,2 hPBG and HbA1c of patients in liraglutide group and metformin hydrochioride group were lower after treatment,and there was significant difference between the two group and the control group after treatment(P ＜ 0.05).BMI of patients in liraglutide group was (24.61 ± 3.47) kg/m2,lower than of the control group((25.37 ± 4.70) kg/m2,P ＜ 0.05).2 hPBG of patients in the liraglutide group was (7.13 ± 3.85)mtmol/L,lower than that of the metformin hydrochioride group ((8.03 ± 4.33) mtmol/L,P ＜ 0.05).FBG level in metformin hydrochioride group ((6.31 ± 3.45) mmol/L) was lower than that of the liraglutide group ((6.98±2.97) mmol/L),but the difference was not statistically significant(P ＞ 0.05).Conclusion Liraglutide and metformin hydrochioride treatment can effectively reduce weight and blood sugar of the overweight diabetics.The effect of liraglutide to reduce postprandial blood glucose and weight of the patient is more significant than of metformin hydrochioride.

Objective To compare the blood glucose level and associated hypoglycemia risks between group of insulin glargine combined with repaglinide and group of mixed insulin in the treatment of type 2 diabetes in the elderly. Methods Sixty four type 2 diabetes patients (age≥60 years) with inadequate glyeaemic control by drugs were divided into 2 groups randomly: glargine group (32 cases) and mixed insulin group (32 cases). In glargine group, 32 patients were given repaglinide before breakfast, lunch, supper respectively and injection of glargine hypodermically once at 22 o'clock every night, while the 32 patients in mixed insulin group were injected with the mixed insulin (Novolin 30R) hypodermically before breakfast and supper respectively for 16 weeks. The dose of repaglinide and insulin were adjusted every 3 days according to the level of fasting glucose (FPG)and postprandial glucose (PPG), reaching the aim of FPG less than 7.2 mmol/L and PPG less than 10mmol/L. The blood glucose level and the incidence of hypoglycemia were observed. Results The daily glucose profile and the level of HbAlc of the 2 groups dropped obviously after 16 weeks treatments (all P<0. 05). At the end of the experiment, the PPG of lunch and supper, and the level of HbAlc were markedly lower in glargine group than in mixed insulin group (all P<0. 05), and the body mass index (BMI) increased markedly in mixed insulin group compared with pre-experiment (P<0. 05), but no significant change was found in glargine group (P>0. 05). The incidence of hypoglycemia in glargine group was lower than that in mixed insulin group (2 patients in glargine group, 12 patients in mixed insulin group, P<0.05). Conclusions Both of the mixed insulin and glargine combined with repaglinide have visible effects on controlling the blood glucose, but the latter has better efficacy, lower risk of hypoglycemia and lower increase of BMI than the former.

Hyperuricemia is the result of purine metabolic or excretion disorder.Continuous hyperuricemia can cause chronic uric acid nephropathy (gouty nephropathy),which will induce varying degrees of renal disfunction and impair life.Uric acid contributes to kidney injury by inducing inflammation,endothelial dysfunction,oxidative stress,and activation of the renin-angiotensin system(RAS),and cause chronic uric acid nephropathy.Thorough tnderstanding of.the pathogenesis of chronic uric acid nephropathy is beneficial for dru development and evaluating disease prognosis.Here,we reviewed of the pathogenesis of chronic uric acid nephropathy.

We reviewed the diagnosis and treatment of three patients with fulminant type 1 diabetes mellitus (FT1D) in our hospital.And then we discussed the clinical characteristics of a total of 24 cases of FT1D from published reports.Among them,14 patients presented with gastrointestinal symptoms.Close attention is needed as FT1D is characterized by acute onset,rapid progression and poor prognosis.

Objective To observe the effect of febuxostat on epithelial-to-mesenchymal transition (EMT) of kidney tubules and the levels of serum IL-6 nad transforming growth factor (TGF) β1 in hyperuricemic rats.Methods Forty male SD rats were divided into 4 groups:normal control group (NC group),oteracil potassium group (OP group),oteracil potassium with febuxostat group (OF group) and oteracil potassium with benzbromarone group (OB group).Each group had 10 rats and balanced in body weights.To induce hyperuricemia,rats were given oteracil potassium by gastric garage once a day for eight weeks.Rats in OF group and OB group were given either febuxostat or benbromarone starting with oteracil potassium,and rats in NC group was given saline only.Blood samples were taken before,and at the end of 4 and 8 weeks of the treatments and serum uric acid,creatinine,blood usea nitrogen (BUN),IL-6 and TGFβ1 contents were measured at each time point.Renal pathological changes were observed via HE and Masson staining,and the expression of α-SMA and E-cadherin were detected by immunohistochemistry.Results Compared with those in NC group,the levels of serum uric acid,creatinine,BUN,IL-6 and TGFβ1 in the another three groups were increased significantly (all P ＜ 0.01).However,the IL-6 and TGFβ1 contents in OF group were much lower than those in OP group (P ＜0.01).HE and Masson staining showed that OF group had less damage and tubulointerstitial fibrosis than OP group and OB group (P ＜0.01).Moreover,the expression of α-SMA was significantly down-regulated (P ＜ 0.01) and that of E-cadherin was significantly up-regulated in OF group compared with those in OP group.Conclusion Febuxostat treatment significantly inhibited EMT and reduced the levels of IL-6 and TGFβ1 in hyperuricemia rats.