Several researches have suggested that estrogen contributes to the initiation and development of thyroid cancer by binding to estrogen receptors (estrogen receptor α,estrogen receptor β,and G-protein-coupled receptor 30),activating gene or non-genomic pathways and regulating proliferation of thyroid cells.Studies on antiestrogen drugs based on inhibiting thyroid cell proliferation may provide a new target in treating thyroid cancer.

Objective To determine the associations of visceral adipose tissue area and retinol binding protein 4(RBP4) with bone mineral density (BMD) in the postmenopausal patients with type 2 diabetes mellitus (T2DM).Methods The cross-sectional study involved 69 postmenopausal patients with T2DM (aged 40-73 years) in our hospital,they were divided into 4 groups:group 1:BMI ＜26.0 kg/m2,VAT＜ 155.3 cm2 ; group 2:BMI ＜ 26.0 kg/m2,VAT＞ 155.3 cm2 ; group 3:BMI ＜26.0 kg/m2,VAT＜155.3 cm2;group 4:BMI＜26.0 kg/m2,VAT＞155.3 cm2.The visceral adipose tissue (VAT) area and subcutaneous adipose tissue (SAT) area were obtained by computed tomography(CT) and BMD was measured by dual energy X-ray absorptiometry (DEXA).Results VAT area had negative associanons with lumbar spine BMD (LS-BMD) and greater trochanter BMD (GT-BMD) (r=-0.367,r=-0.301),and with LS-BMD,GT-BMD,femoral neck BMD (FN-BMD) and intertrochanter BMD (IT-BMD) even after adjusting for body mass index(BMI) and SAT (r =-0.433,-0.432,-0.300,-0.297,all P＜0.05).A negative relationship was showed between LNRBP4 and LS-BMD in postmenopausal female patients (all P ＜ 0.05.) The postmenopausal female patients with T2DM were divided into four groups according to the mean values of BMI and VAT area.BMD at any site of group 3(LS-BMD:1.00±0.20,FN-BMD:0.82±0.17,IT-BMD:1.13±0.21,GT-BMD:0.76±0.18) were higher than group 2(0.79±0.14,0.70±0.10,0.95±0.14,0.58±0.11).The multiple regression indicated that the variation of predictors (age,DUR,BMI,VAT,HbA1c,FINS and PMT) explained 51.7％,52.2％,59.8％ and 75.3％ of the variation in LS-BMD.FN-BMD,IT-BMD,GT-BMD among subjects,respectively(all P＜0.01).Conclusions The influence of fat on bone density may depend on its site of VAT or SAT.VAT could be an independent determinant factor of BMDin the postmenopausal female with T2DM.Serum RBP4 may contribute to this effect.

The changes of the levels of C-reactive protein,endothelin and nitric oxide before and after pioglitazone treatment in type 2 diabetic patients suggested that inflammation participated in the pathogenesis of diabetic macroangiopathy and pioglitazone can protect vessels

Forty-five male SD rats were divided into normal group, diabetic control group, and rosiglitazone treatment diabetic group.By the end of 12 weeks, the expressions of pigment epithelium-derived factor(PEDF), matrix metalloproteinase-2 (MMP-2), and transforming growth factor-β1 (TGF-β1) in the kidney were determined by immunohistochemistry and RT-PCR.The results showed that rosiglitazone decreased the increased kidney weight/body weight ratio, serum creatinine, blood ureanitrogen, urinary albumin excretion, triglyceride levels in diabetic rats (all P＜0.01).Rosiglitazone prevented the decreasing of protein expressions of PEDF and MMP-2 and the increasing of protein expression of TGF-β1 (all P＜0.01).PEDF mRNA showed a similar change,suggesting that renoprotection of rosiglitazone on diabetic rats may be mediated through regulating the expressions of PEDF, MMP-2, and TGF-β1.

Obesity is not only the high risk factor of diabetes mellitus,coronary heart disease and hypertension,but also a cause of renal damage.Diabetic nephropathy is one of the most frequent chronic microvascular complications of diabetes mellitus,and one of the leading causes of end-stage kidney failure.It is documented that the obese patients with type 2 diabetes may have obviously multiple metabolic abnormalities and are more prone to develop diabetic nephropathy.This article summarized the pathogenetic mechanisms of kidney injury in diabetic obese patients and provided some ideas in the medical therapy of diabetic nephropathy.

Objective To investigate the functional mechanism of metformin in improving the fatty liver and the treatment of the relative metabolic abnormalities of type 2 diabetes mellitus.Methods The model of type 2 diabetes mellitus complicated with fatty liver was set up by feeding high-glucose-high-fat diet and by injecting STZ.Then,the rats were made an intervention with metformin.At the end of 4 weeks and 8 weeks,the fasting blood glucose,the level of fasting serum insulin.At the end of 18 weeks the fasting blood glucose,the level of fasting serum insulin,ALT,TNF-? and the level of leptin of every group of rats were measured and the expression of TNF-? in the liver was determined.Results Metformin could largely reduce the blood glucose,TG,TC and the fatty content of the liver,improve the state of the insulin resistance and reduce the expression level of the TNF-? in the liver.Conclusion Metformin can have the treatment functions to the rats with fatty liver in the model of type 2 diabetes mellitus complicated with fatty liver.

Objective To investigate the relationship between l evels of FⅦc and features of IR as well as macrovascular complications in type 2 diabetes.Methods The 2001-10~2002-08 FⅦc levels were measured by a one -stage biological assay in patients with type 2 diabetes and controls.Results (1)Type 2 diabetic patients had significantly higher FⅦc than control subjects.(2)FⅦc levels were higher in the type 2 diabetes w ith macrovascular complications than in those without macrovascular complication s.(3)FⅦc levels correlated positively with most features of IR.Conclusion FⅦc levels are increased in type 2 diabetic pat ients.Elevated FⅦc may be an important sign of IR and may contribute to type 2 diabetes and its macrovascular diseases.

Objective To investigate the relationship between serum Leptin levels and insulin resistance.Methods During 2001-10~2002-08 fasting serum Leptin concentrations were measured with RIA in 196 cases(including 118 type 2 diabetes,78 controls),and height,body weight were measured to calculate body mass index(BMI).Results HbA_1c,SBP,TG,Leptin were correlated with ISI,Leptin concentration were higher in type 2 diabetes than in controls;Leptin concentration was significantly increased in obese subjects,whereas in type 2 diabetes serum Leptin concentration had no significant difference between obese subjects and non-obese subjects.Conclusion Most of obeses subjects have insulin resistance,whether obesity or not,the patients type 2 diabetes have some kind of insulin resistance.

Objective To compare the safety and efficacy of insulin degludec (IDeg) with those of insulin glargine (IGlar) in insulin-naive subjects with type 2 diabetes (T2DM).Methods This was a 26-week,randomized,open-label,parallel-group,treat-to-target trial in 560 Chinese subjects with T2DM (men/women:274/263,mean age 56 years,mean diabetes duration 7 years) inadequately controlled on oral antidiabetic drugs (OADs).Subjects were randomized 2:1 to once-daily IDeg (373 subjects) or IGlar(187 subjects),both in combination with metformin.The primary endpoint was changes from baseline in glycosylated hemoglobin(HbA1c) after 26 weeks.Results Mean HbA1c decreased from 8.2％ in both groups to 6.9％ in IDeg and 7.0％ in IGlar,respectively.Estimated treatment difference (ETD) of IDegIGlar in change from baseline was-0.10％ points (95％ CI-0.25-0.05).The proportion of subjects achieving HbA1c ＜ 7.0％ was 56.3％ and 49.7％ with IDeg and IGlar,respectively [estimated odds ratio of IDeg/IGlar:1.26 (95 ％ CI 0.88-1.82)].Numerically lower rateof overall confirmed hypoglycaemia and statistically significantly lower nocturnal confirmed hypoglycemia were associated with IDeg compared with IGlar,respectively [estimated rateratio of IDeg/IGlar 0.69 (95％ CI 0.46-1.03),and 0.43 (95％ CI 0.19-0.97)].No differences in other safety parameters were found between the two groups.Conclusions IDeg was non-inferior to IGlar in terms of glycaemic control,and was associated with a statistically significantly lower rate of nocturnal confirmed hypoglycaemia.IDeg is considered to be suitable for initiating insulin therapy in Chinese T2DM patients on OADs requiring intensified treatment.Clinical trail registration Clinicaltrials.gov,NCT01849289.