To investigate the effect of angiotensin receptor blocker ( ARB ) telmisartan on endoplasmic reticulum stress -related kidney cells apoptosis in diabetic rats.31 male SD rats were divided into 3 groups:normal control group,diabetic group,and telmisartan treated diabetic group.After 12 weeks' experiment,weight,24 h urinary albumin excretion,blood glucose,serum insulin,and serum creatinine were determined.Renal cell apoptosis was examined by using TUNEL; Renal cell endoplasmic reticulum stress signaling pathway molecules glucose regulated protien 78 ( GRP78 ),caspase12,and CHOP were detected with immunohistochemistry and realtime PCR.24 h urine protein and serum creatinine in diabetic group were significantly higher than those in the control group; while body weight and plasma insulin were significantly lower than those in the control group( P＜0.05 ) ;Compared with diabetic group,24 h urinary protein and serum creatinine were decreased significantly in telmisartan treated diabetic group( P＜0.05 ).The apoptosis index of telmisartan treated group was significantly lower than that of diabetic group( P＜0.05 ).Endoplasmic reticulum stress signaling pathway molecules GRP78,caspase12,CHOP protein and mRNA expression in diabetic group were significantly higher than those in control group( P＜0.05 ),as well as in telmisartan treated group( P＜0.05 ).Endoplasmic reticulum stress took part in kidney cell apoptosis of the diabetic rat.Telmisartan possessed a protective effect on endoplasmic reticulum stress-related renal cells apoptosis.

Objective To assess the coordinated regulation and the molecular mechanisms of 17β-estradiol and 1,25-dihydroxyvitamin D3 [ 1,25-( OH ) 2 D3 ] on the proliferation and differentiation of osteoblastic MC3T3-E1 cells.Methods MC3T3-E1 cells were cultured in phenol-red free α-MEM medium supplemented with 10％ FBS,MTT assay was performed to determine the effects of 17β-estradiol and 1,25-( OH )2 D3 on MC3T3-E1 cells proliferation.After cells were treated with different agents,cell cycle related genes [ cyclin E,proliferation cell nuclear antigen ( PCNA ),and cyclin-dependent kinase inhibitor 2b ( Cdkn2b ) ] and markers of osteoblastic differentiation [ type Ⅰ collagen ( COL Ⅰ ),alkaline phosphatase ( ALP),osteopontin ( OPN ) ] were detected with SYBR green-based quantitative PCR.ALP activity was detected with BCIP/NBT method.Results 17β-estradiol could promote proliferation of MC3T3-E1 cells,which was accordant to its ability to increase cyclin E and PCNA and to inhibit Cdkn2b mRNA expression in MC3T3-E1 cells.However,1,25-( OH)2D3 had no effect on the proliferation of MC3T3-E1 cells and also did not enhance the proliferation of MC3T3-E1 cells stimulated by 17β-estradiol.On the other hand,17β-estradiol promoted the gene expression of differentiation markers Col Ⅰ,ALP,and OPN,and 1,25-(OH) 2 D3 synergistically increased the expression of these genes with 17 β-estradiol.Conclusion As two of the most important hormones which regulate bone metabolism,estrogen and vitamin D may coordinately promote osteoblast differentiation,but may not regulate osteoblasts proliferation synergistically.

Ninty-eight patients of type 2 diabetes mellitus with mild cognitive impairment were collected according to the Montreal Cognitive Assessment( MoCA )and mismatch negativity( MMN ).Forty-eight patients were assigned to conventional treatment with nimodipine (20 mg/d).The MoCA and MMN were evaluated and compared with the remaining 50 patients who served as a control group.There was no significant difference between two patient groups in MoCA( P＞0.05 ) ;the latency and amplitude of MMN were significantly improved in the treated group( P＜0.05 ) ; the amplitude of MMN was reduced in control group ( P＜0.05 ),but the latency of MMN showed no significant change( P＞0.05 ).

Insulin autoimmune syndrome (IAS) is rare.A patient with IAS was herewith reported and 50domestic cases reported in the last two decades were reviewed to discuss the approach to this syndrome.In hypoglycemic patients with high insulin level and with Graves' disease and taking tapazole,insulin autoantibody detection is mandatory to avoid misdiagnosis and unnecessary surgery.

The failure of islet β cell is the core pathogenic mechanism of diabetes,which is also the key target for type 2 diabetic mellitus treatment.A large amount of basic and clinical researches have been confirmed that glucagon like peptide-1 and its analogue liraglutide have abilities to significantly improve islet β cell function besides the glucose-dependent lowering hyperglycemia effects.Furthermore,liraglutide is approved to improve β cell function,thus providing a new choice for treatment of type 2 diabetes.

Vildagliptin is a potent and specific inhibitor of dipeptidyl peptidase 4,which has been implicated to enhance and prolong the physiological actions of incretion hormones including glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide.Vildagliptin is an orally administered drug and has been licensed for the treatment of type 2 diabetes mellitus.Vildagliptin monotherapy or in combination with other drugs can effectively lower glycosylated haemoglobin levels to a great extent.In addition,vildagliptin acts in a glucose-dependent manner,explaining its low risk of hypoglycemia.This drug has been proved well tolerated with few gastrointestinal side effects or oedema.Therefore vildagliptin is a promising new option for type 2 diabetic patients,and these patients would achieve better glycemic control and fewer complications in the long run.

ObjectiveTo investigate the risk factors of metabolic syndrome ( MS ) in obese subjects.Methods A seven-year follow-up study was conducted in 413 simple obese subjects and 196 subjects with normal body weight who were recruited from community residents during physical examination in 2000.There was a 7 years follow-up.Anthropometrics,blood pressure,lipid profile,fasting blood glucose,and 2 h blood glucose after glucose loading were measured.Endothelium-dependent dilatation (EDD) test was also performed.Results Among 553 of 609 subjects who were followed up in 2007,there were 381 simple obese subjects ( simple obese group) and 172 normal weight subjects( normal weight group).Seven-year cumulative incidence of MS was 35.17％ in simple obese group and 8.14％ in normal weight group.In simple obese group,subjects with MS showed greater or higher levels of waist circumference( WC ),waist-hip ratio ( WHR ),triglyceride ( TG ),fasting plasma glucose ( FPG ),fasting insulin (FINS),and homeostasis model assessment for insulin resistance index (HOMA-IR) (all P＜0.05 ),and also decreased EDD( P＜0.05 ) as compared with those without MS.WC,WHR,and FINS were higher( all P＜0.05 ) and EDD was lower( P＜0.05 ) in subjects with MS of normal weight group than those without MS.Logistic analysis showed that the male gender,WC,WHR,FPG,HOMA-IR,and EDD were major risk factors of MS.Conclusion Central obesity,insulin resistance,and endothelial dysfunction are important independent risk factors for development of MS.

Objective To investigate the prevalence of depression and its risk factors in type 2 diabetes mellitus.Methods Beck Depression Inventory (BDI) was used to evaluate depression in 2 966 type 2 diabetes mellitus patients [ male 1 463,female 1 503,age ( 56.4 ± 11.2 ) years,diabetes duration ( 6.3 ± 5.7 ) years ].Depression criteria:≤4 points,no depression group; 5-13 points,mild depression group; 14-20 points,moderate depression group; 21 points or higher,severe depression group.Meanwhile,the demographic and metabolic data and diabetes-related health behaviors were also investigated.The risk factors associated with depression were screened by logistic regression.Results 51％ patients had depression,including 38％ with mild,8％ with moderate,and 5％ with severe depression.Compared with no depression group,depression was correlated with female sex,low-annual income,diabetes education,diabetes treatment,with insulin and peripheral neuropathy( P＜0.01 ).More smoking and younger age were found in severe depression( P＜0.05 ).Partial correlation analysis showed that depression in type 2 diabetes mellitus was positively correlated with female sex,diabetes education,and peripheral neuropathy ; and negatively correlated with age (P＜0.05).Conditional logistic regression equation showed that gender( OR =1.37 ),age ( 20-40 years,OR =1.52 ),diabetes education ( OR =1.51 ),and peripheral neuropathy ( OR =1.87 ) were risk factors for depression.Conclusion Depression is common in type 2 diabetes mellitus.More attention should be paid to screening depression in clinical practice.

Increasing clinical evidence shows that modern lifestyle interrupting circadian rhythm contributes to the prevalence of obesity and diabetes.Recent genetic animal models further support the interaction of circadian rhythms and metabolic state.Circadian clock is not limited to be in central nervous system,and is also present in nearly all cells of the body,which constitute hierarchically circadian systems.The molecular circadian clock is evolved to allow organisms to anticipate and prepared for predictable,daily changes in the environment and regulates cellular and tissue function by driving patterns of gene expression and enzymatic activity.At present,basic science in this field has progressed at an extraordinary pace and is expected to continue unraveling the mechanisms linking circadian clocks to metabolism,which is important for understanding the pathophysiology of metabolic diseases such as obesity and diabetes,and provides a conceptual basis for the prevention and therapeutics of these diseases.

Patients with acute myocardial infarction(AMI) are often with elevated blood glucose level when admitted to hospital,this finding is associated with poor prognosis regardless of a history of diabetes.Though numerous studies have addressed some of the questions in this field,many critically important questions are still poorly understood and under debate.This article summarized current findings in hyperglycemia and its potential link withadverse outcomes in AMI patients,and addressed some of the existing controversies in this field.