Efficacy and safety of bexagliflozin compared with dapagliflozin as an adjunct to metformin in Chinese patients with type 2 diabetes mellitus: A 24-week, randomized, double-blind, active-controlled, phase 3 trial.

BACKGROUND: Bexagliflozin and dapagliflozin are sodium-glucose cotransporter-2 (SGLT2) inhibitors. No direct comparison of SGLT2 inhibitors in a randomized controlled trial has been reported to date. METHODS: This was a multicenter, randomized, double-blind, active-controlled trial comparing bexagliflozin to dapagliflozin for the treatment of type 2 diabetes mellitus in adults with disease inadequately controlled by metformin. Subjects (n = 406) were randomized to receive bexagliflozin (20 mg) or dapagliflozin (10 mg) plus metformin. The primary endpoint was noninferiority of bexagliflozin to dapagliflozin for the change in glycated hemoglobin (HbA1c) from baseline to week 24. Secondary endpoints included intergroup differences in fasting plasma glucose (FPG), 2-h-postprandial glucose (PPG), body weight, and systolic blood pressure (SBP) from baseline to week 24. The trial also evaluated the safety profiles. RESULTS: The model-adjusted mean change from baseline to week 24 HbA1c was -1.08% for bexagliflozin and -1.10% for dapagliflozin. The intergroup difference of 0.03% (95% confidence interval [CI] -0.14% to 0.19%) was below the prespecified margin of 0.4%, confirming the noninferiority of bexagliflozin. The changes from baseline in FPG, PPG, body weight, and SBP were -1.95 mmol/L, -3.24 mmol/L, -2.52 kg, and -6.4 mm Hg in the bexagliflozin arm and -1.87 mmol/L, -3.07 mmol/L, -2.22 kg, and -6.3 mm Hg in the dapagliflozin arm. Adverse events were experienced in 62.6% and 65.0% and serious adverse events affected 4.4% and 3.5% of subjects in the bexagliflozin and dapagliflozin arm, respectively. CONCLUSIONS: Bexagliflozin showed nearly identical effects and a similar safety profile to dapagliflozin when used in Chinese patients on metformin.

Supplementation of Schisandrin B in Semen Extender Improves Quality and Oxidation Resistance of Boar Spermatozoa Stored at 4 °C.

During cold storage, boar spermatozoa undergo oxidative stress, which can impair sperm function and fertilizing capacity. The objective of the present study was to assess the effects of Schisandrin B (Sch B) in semen extenders on the quality of boar semen stored at hypothermia. Semen was collected from twelve Duroc boars and diluted in extenders supplemented with different concentrations of Sch B (0 µmol/L, 2.5 µmol/L, 5 µmol/L, 10 µmol/L, 20 µmol/L, and 40 µmol/L). Here, we demonstrated that 10 µmol/L Sch B provided the best effects on motility, plasma membrane integrity, acrosome integrity, sperm normality rate, average movement velocity, wobbility, mitochondrial membrane potential (MMP), and DNA integrity of sperm. The results of Sch B effects on antioxidant factors in boar sperm showed that Sch B significantly elevated the total antioxidant capacity (T-AOC) and markedly decreased the reactive oxygen species (ROS) and malondialdehyde (MDA) content of sperm. The expression of catalase (CAT) and superoxide dismutase (SOD) mRNA was increased, while the expression of glutathione peroxidase (GPx) mRNA demonstrated no change compared to non-treated boar sperm. Compared to the non-treated group, Sch B triggered a decrease in Ca2+/protein kinase A (PKA) and lactic acid content in boar sperm. Similarly, Sch B led to a statistically higher quantitative expression of AWN mRNA and a lower quantitative expression of porcine seminal protein I (PSP-I) and porcine seminal protein II (PSP-II) mRNA. In a further reverse validation test, no significant difference was observed in any of the parameters, including adhesion protein mRNA, calcium content, lactic acid content, PKA, and protein kinase G (PKG) activity after sperm capacitation. In conclusion, the current study indicates the efficient use of Sch B with a 10 µmol/L concentration in the treatment of boar sperm through its anti-apoptosis, antioxidative, and decapacitative mechanisms, suggesting that Sch B is a novel candidate for improving antioxidation and decapacitation factors in sperm in liquid at 4 °C.

Metformin prevents methylglyoxal-induced apoptosis by suppressing oxidative stress in vitro and in vivo.

Methylglyoxal (MGO) is an active metabolite of glucose and plays a prominent role in the pathogenesis of diabetic vascular complications, including endothelial cell apoptosis induced by oxidative stress. Metformin (MET), a widely prescribed antidiabetic agent, appears to reduce excessive reactive oxygen species (ROS) generation and limit cell apoptosis. However, the molecular mechanisms underlying this process are still not fully elucidated. We reported here that MET prevents MGO-induced apoptosis by suppressing oxidative stress in vitro and in vivo. Protein expression and protein phosphorylation were investigated using western blotting, ELISA, and immunohistochemical staining, respectively. Cell viability and apoptosis were assessed by the MTT assay, TUNEL staining, and Annexin V-FITC and propidium iodide double staining. ROS generation and mitochondrial membrane potential (MMP) were measured with fluorescent probes. Our results revealed that MET prevented MGO-induced HUVEC apoptosis, inhibited apoptosis-associated biochemical changes such as loss of MMP, the elevation of the Bax/Bcl-2 ratio, and activation of cleaved caspase-3, and attenuated MGO-induced mitochondrial morphological alterations in a dose-dependent manner. MET pretreatment also significantly suppressed MGO-stimulated ROS production, increased signaling through the ROS-mediated PI3K/Akt and Nrf2/HO-1 pathways, and markedly elevated the levels of its downstream antioxidants. Finally, similar results were obtained in vivo, and we demonstrated that MET prevented MGO-induced oxidative damage, apoptosis, and inflammation. As expected, MET reversed MGO-induced downregulation of Nrf2 and p-Akt. In addition, a PI3K inhibitor (LY-294002) and a Nrf2 inhibitor (ML385) observably attenuated the protective effects of MET on MGO-induced apoptosis and ROS generation by inhibiting the Nrf2/HO-1 pathways, while a ROS scavenger (NAC) and a permeability transition pores inhibitor (CsA) completely reversed these effects. Collectively, these findings broaden our understanding of the mechanism by which MET regulates apoptosis induced by MGO under oxidative stress conditions, with important implications regarding the potential application of MET for the treatment of diabetic vascular complications.

Effectiveness of cognitive behavior therapy for sleep disturbance and glycemic control in persons with type 2 diabetes mellitus: A community-based randomized controlled trial in China.

BACKGROUND: Poor sleep quality is a common clinical feature in patients with type 2 diabetes mellitus (T2DM), and often negatively related with glycemic control. Cognitive behavioral therapy (CBT) may improve sleep quality and reduce blood sugar levels in patients with T2DM. However, it is not entirely clear whether CBT delivered by general practitioners is effective for poor sleep quality in T2DM patients in community settings. AIM: To test the effect of CBT delivered by general practitioners in improving sleep quality and reducing glycemic levels in patients with T2DM in community. METHODS: A cluster randomized controlled trial was conducted from September 2018 to October 2019 in communities of China. Overall 1033 persons with T2DM and poor sleep quality received CBT plus usual care or usual care. Glycosylated hemoglobin A1c (HbAlc) and sleep quality [Pittsburgh Sleep Quality Index (PSQI)] were assessed. Repeated measures analysis of variance and generalized linear mixed effects models were used to estimate the intervention effects on hemoglobin A1c and sleep quality. RESULTS: The CBT group had 0.64, 0.50, and 0.9 lower PSQI scores than the control group at 2 mo, 6 mo, and 12 mo, respectively. The CBT group showed 0.17 and 0.43 lower HbAlc values than the control group at 6 mo and 12 mo. The intervention on mean ΔHbAlc values was significant at 12 mo (t = 3.68, P < 0.01) and that mean ΔPSQI scores were closely related to ΔHbAlc values (t = 7.02, P < 0.01). Intention-to-treat analysis for primary and secondary outcomes showed identical results with completed samples. No adverse events were reported. CONCLUSION: CBT delivered by general practitioners, as an effective and practical method, could reduce glycemic levels and improve sleep quality for patients with T2DM in community.

Effect of group cognitive behavioural therapy on psychological stress and blood glucose in people with type 2 diabetes mellitus: A community-based cluster randomized controlled trial in China.

OBJECTIVE: To assess whether group cognitive behavioural therapy (GCBT) delivered by general practitioners reduces anxiety and depression and improves glycaemic levels in adults with type 2 diabetes mellitus. METHODS: We conducted a community-based cluster randomized controlled trial in adults with type 2 diabetes mellitus from 48 communities in China. Participants received either GCBT plus usual care (UC) or UC only. General practitioners were trained in GCBT before intervention in the intervention group. The primary outcome was glycated haemoglobin (HbA1c ) concentration. Outcome data were collected from all participants at baseline, 2 months, 6 months and 1 year. The secondary outcomes were depression (Patient Health Questionnaire-9; PHQ-9) and anxiety (General Anxiety Disorder questionnaire; GAD-7). RESULTS: The GCBT group showed greater improvement in GAD-7 and PHQ-9 scores, respectively, than the UC group after 2 months post-baseline (T = -6.46, p < 0.0001; T = -5.29, p < 0.001), 6 months (T = -4.58, p < 0.001; T = -4.37, p < 0.001) and 1 year post-intervention (T = -3.91, p < 0.001; T = -3.57, p < 0.001). There was no difference in HbA1c values between the GCBT and UC groups at 2 months while the values were lower in the GCBT group at 6 months and 1 year (T = -6.83, p < 0.001; T = -4.93, p < 0.001, respectively). Subgroup analysis indicated a long-term effect of GCBT only for mild and moderate anxiety and mild depression groups. Similarly, HbA1c values reduced only in the mild and moderate anxiety and the mild depression groups. CONCLUSIONS: General practitioners can deliver GCBT interventions. GCBT plus UC is superior to UC for reducing mild/moderate anxiety and depression, and improving glycaemic levels. TRIAL REGISTRATION: Chinese clinical trials registration (ChiCTR-IOP-16008045).

Facile and Safe Synthesis of Novel Self-Pored Amine-Functionalized Polystyrene with Nanoscale Bicontinuous Morphology.

The chloromethyl-functionalized polystyrene is the most commonly used ammonium cation precursor for making anion exchange resins (AER) and membranes (AEM). However, the chloromethylation of polystyrene or styrene involves highly toxic and carcinogenic raw materials (e.g., chloromethyl ether) and the resultant ammonium cation structural motif is not stable enough in alkaline media. Herein, we present a novel self-pored amine-functionalized polystyrene, which may provide a safe, convenient, and green process to make polystyrene-based AER and AEM. It is realized by hydrolysis of the copolymer obtained via random copolymerization of N-vinylformamide (NVF) with styrene (St). The composition and structure of the NVF-St copolymer could be controlled by monomeric ratio, and the copolymers with high NVF content could form bicontinuous morphology at sub-100 nm levels. Such bicontinuous morphology allows the copolymers to be swollen in water and self-pored by freeze-drying, yielding a large specific surface area. Thus, the copolymer exhibits high adsorption capacity (226 mg/g for bisphenol A). Further, the amine-functionalized polystyrene has all-carbon backbone and hydrophilic/hydrophobic microphase separation morphology. It can be quaternized to produce ammonium cations and would be an excellent precursor for making AEM and AER with good alkaline stability and smooth ion transport channels. Therefore, the present strategy may open a new pathway to develop porous alkaline stable AER and AEM without using metal catalysts, organic pore-forming agents, and carcinogenic raw materials.

Interaction of sleep quality and anxiety on quality of life in individuals with type 2 diabetes mellitus.

PURPOSE: Sleep disturbances and anxious symptoms are very common in people with type 2 diabetes mellitus(T2DM). This study aimed to assess the interactive effects of poor sleep quality and anxious symptoms on the quality of life of people with T2DM. METHODS: Nine hundred and forty-four participants with T2DM were enrolled in a cross-sectional study. Demographic and physiological characteristics were recorded. Each participant completed a Chinese version of the Pittsburgh Sleep Quality Index, the Patient Health Questionnaire-9 and General Anxiety Disorder questionnaire, and the Diabetes Specificity Quality of Life scale. The products of poor sleep quality and anxiety were added to a logistic regression model to evaluate the multiplicative interactions, expressed as the relative excess risk of interaction, the attributable proportion of interaction, and the synergy index. RESULTS: Poor sleep quality and anxiety symptoms were associated with reduced quality of life. There was a significant interaction between poor sleep quality and anxiety symptoms; this combined effect significantly reduced quality of life scores by 6.09-fold. The relative excess risk of interactions was 1.36. CONCLUSIONS: The combined effect of poor sleep quality and anxiety symptoms reduces quality of life in people with T2DM. TRIAL REGISTRATION: ChiCTR-IOP-16008045. Registered 3 March 2016. A clinical study to investigate gum infection in patients undergoing kidney dialysis.

Interactive effect of sleep duration and sleep quality on risk of stroke: An 8-year follow-up study in China.

Inappropriate sleep duration and poor sleep quality are associated with risk of stroke, but their interactive effect on stroke is unknown. We explored the interactive effect of sleep quality and duration on stroke risk. A prospective cohort study was conducted with 41,786 adults. Sleep quality was assessed using the Pittsburgh Sleep Quality Index. Sleep duration was measured by average hours of sleep per night. Cox regression models were used to calculate the association of sleep duration and quality with stroke. The delta method and a non-conditional logistic regression model were used and the relative excess risk due to interaction (RERI), the attributable proportion (AP), and the synergy index (S) were calculated. Compared with sleep duration 6-8 h/day, the risk ratio of stroke was 1.63 (1.23-2.11) times for sleep duration <6 h/day and 1.40 (1.08-1.75) times for >8 h/day. The stroke risk ratio was 2.37 (1.52-3.41) times in subjects with poor sleep quality compared with those with good sleep quality. Women who slept <6 h/day had higher stroke risk than men who slept <6 h/day. Men who slept >8 h/day had higher stroke risk than women who slept >8 h/day. Men with poor sleep quality had higher stroke risk than women with poor sleep quality. Stroke was associated with short/long sleep duration and poor sleep quality in subjects aged >46 years, compared with those aged 18-45 years. Stroke occurred more frequently in subjects with poor sleep quality combined with short sleep duration (odds ratio: 6.75; 95% confidence interval (CI): 2.45-14.12). RERI, AP, and S values (and their 95% CIs) were 5.54 (3.75-8.12), 0.72 (0.56-0.80), and 5.69 (4.23-9.90) for the poor sleep quality interact with short sleep duration. In persons with poor sleep quality accompanied by long sleep duration, RERI, AP, and S (95% CI) were 1.12 (1.01-1.27), 0.35 (0.26-0.51), and 2.05 (1.57-2.96), respectively. Subjective sleep disturbances are related with risk of stroke in Chinese adults. There are additive interactions between short/long sleep duration and poor sleep quality that affect risk of stroke.

Prolonged therapeutic effects of photoactivated adipose-derived stem cells following ischaemic injury.

AIM: Adipose-derived stem cells (ASCs) therapies are emerging as a promising approach to therapeutic angiogenesis. Therapeutic persistence and reduced primitive stem cell function following cell delivery remains a critical hurdle for the clinical translation of stem cells in current approaches. METHODS: Cultured ASCs were derived from subcutaneous white adipose tissue isolated from mice fed a normal diet (ND). Unilateral hindlimb ischaemia model was induced in high-fat diet (HFD)-fed mice by femoral artery interruption, after which photoactivated and non-light-treated ASCs were injected into the tail vein of mice. Laser Doppler imaging was conducted to measure the blood flow reperfusion. Capillary density was measured in the ischaemic gastrocnemius muscle. mRNA levels of angiogenic factors were determined by reverse-transcription polymerase chain reaction. Flow cytometry was used to determine the characterization of ASCs and endothelial progenitor cell (EPC). Human ASCs secretomes were analysed by liquid chromatography tandem mass spectrometry. RESULTS: Our study demonstrated that photoactivated ND-ASCs prolonged functional blood flow perfusion and increased ASCs-derived EPC and neovascularization 38 days after ligation, when compared with saline-treated controls. Profiling analysis in ischaemic muscles showed upregulation of genes associated with pro-angiogenic factors after injection of photoactivated ND-ASCs when compared with the non-light-treated ASCs or saline treated HFD mice. Mass spectrometry revealed that light-treated ASCs conditioned medium retained a more complete pro-angiogenic activity with significant upregulation of angiogenesis related proteins. CONCLUSION: Our data demonstrates that photoactivated ND-ASCs improve blood flow recovery and their injection may prove to be a useful strategy for the prevention and treatment of diabetic peripheral arterial disease.

Transplantation of adipose tissue lacking PAI-1 improves glucose tolerance and attenuates cardiac metabolic abnormalities in high-fat diet-induced obesity.

Adipose tissue is an important metabolic organ, and transplantation of white adipose tissue plays crucial roles in glucose homoeostasis and energy metabolism. However, how adipose tissue affects glucose utilization is poorly understood. PAI-1-knockout (PAI-1KO) mice were previously shown to be resistant to a high-fat diet and obesity. We used microPET/CT (positron emission tomography/computed tomography), gene microarray, and biochemical assays to measure changes in systemic and myocardial glucose metabolism in mice subjected to transplantation of adipose tissue from PAI-1KO and wild-type mice. Here, we show that transplanting subcutaneous white adipose tissue (scWAT) from PAI-1KO mice into high-fat diet (HFD)-fed mice reduced levels of serum total cholesterol and triglycerides, and improved glucose tolerance in the HFD-fed mice. microPET/CT imaging revealed that cardiac glucose uptake was increased in the heart but not in the liver, hindlimb muscles, or abdominal subcutaneous white adipose tissue in HFD-fed mice transplanted with PAI-1KO scWAT, suggesting that the transplanted PAI-1KO scWAT exerted endocrine effects in the heart. In addition, transplantation of scWAT from PAI-1KO mice upregulated mitochondrial gene expression in cardiac muscle, increased the expression of glucose transporters 1 and 4 in cardiac tissues and was associated with an increased NAD+/NADH ratio. Together, these findings suggest that modulating PAI-1 in scWAT may provide a promising approach for intervening in glucose metabolism.

Circulating miR-103 family as potential biomarkers for type 2 diabetes through targeting CAV-1 and SFRP4.

AIMS: MicroRNA-103 (miR-103) family plays important roles in regulating glucose homeostasis in type 2 diabetes mellitus (DM2). However, the underlying mechanisms remain poorly characterized. The objective of this study was to test the hypothesis that circulating miR-103a and miR-103b, which regulate CAV-1 and SFRP4, respectively, are novel biomarkers for diagnosis of DM2. METHODS: We determined the predictive potential of circulating miR-103a and miR-103b in pre-DM subjects (pre-DM), noncomplicated diabetic subjects, and normal glucose-tolerance individuals (control) using bioinformatic analysis, qRT-PCR, luciferase assays, and ELISA assays. RESULTS: We found that both miR-103a and miR-103b had high complementarity and conservation, modulated reporter gene expression through seed sequences in the 3'UTRs of CAV-1 and SFRP4 mRNA, and negatively regulated their mRNA and protein levels, respectively. We also found that increased miR-103a and decreased miR-103a in plasma were significantly and negatively correlated with reduced CAV-1 levels and elevated SFRP4 levels in pre-DM and DM2, respectively, and were significantly associated with glucose metabolism, HbA1c levels, and other DM2 risk factors for progression from a normal individual to one with pre-DM. Furthermore, we demonstrated that the reciprocal changes in circulating miR-103a and miR-103b not only provided high sensitivity and specificity to differentiate the pre-DM population but also acted as biomarkers for predicting DM2 with high diagnostic value. CONCLUSIONS: These findings suggest that circulating miR-103a and miR-103b may serve as novel biomarkers for diagnosis of DM2, providing novel insight into the mechanisms underlying pre-DM.

Circulating miR-30c as a predictive biomarker of type 2 diabetes mellitus with coronary heart disease by regulating PAI-1/VN interactions.

AIMS: Type 2 diabetes mellitus (DM2) is associated with coronary heart disease (CHD) and is characterized by high levels of plasminogen activator inhibitor (PAI)-1. Circulating microRNAs have been reported as potential diagnostic biomarkers for DM2 and CHD. However, the underlying mechanisms have largely remained unclear. MAIN METHODS: The changes of circulating miR-30c, PAI-1 and vitronetin (VN) in plasma from CHD, noncomplicated (NC) + DM2, CHD + DM2 subjects and control individuals were assessed by quantitative reverse transcription PCR (qRT-PCR) and ELISA assays, respectively. The effects of miR-30c on VN expression by targeting PAI-1 were assessed in vitro SMC and in ex vivo plasma, using bioinformatic analysis, miRNA transfection, luciferase assays, qRT-PCR and western blot, respectively. KEY FINDINGS: We found that decreased circulating miR-30c was negatively correlated with the severity of coronary lesions and the resulting elevated PAI-1 and VN levels. Circulating miR-30c significantly distinguished between patients with CHD + DM2, NC + DM2, CHD and control subjects, and that were significantly associated with certain risk factors for progression from a normal individual to one with CHD + DM2. Furthermore, we also showed that miR-30c plays a previously unrecognized role in regulating the expression of VN levels via regulating PAI-1 levels in vitro SMC and in ex vivo plasma. SIGNIFICANCE: These findings provide a novel regulatory mechanism of miR-30c in regulating PAI-1/VN interactions and that may serve as a diagnostic biomarker of DM2 that is complicated with CHD.

Relationship between subjective sleep disturbances and glycaemia in Chinese adults with type 2 diabetes: findings from a 1.5-year follow-up study.

We wanted to determine whether subjective sleep disturbance was associated with serum glycated hemoglobin (HbA1c) in people with type 2 diabetes mellitus. In total, 944 randomly-selected people with diabetes completed the Chinese version of the Pittsburgh Sleep Quality Index (PSQI). Participants' glycaemia was assessed using HbA1c in March 2016 and September 2017. The PSQI score and the change in score(△PSQI), and the HbA1c and its change (△HbAlc) were analysed by sex and age (30-45, 46-60, 61-75, and 76-89 years). Associations between time point PSQI and △PSQI with static HbA1c and △HbA1c were analysed using multiple linear regression. The results showed subjective sleep disturbance among people with diabetes was not correlated with serum HbAlc (ß coefficient = 0.032, P = 0.103). However, cross-sectional multiple linear regression showed the relationship was present in women (ß coefficient = 0.163, P < 0.01). In multiple linear regression, △PSQI score was correlated with △HbAlc value (ß coefficient = 0.142, P < 0.01). The regression coefficient (ß) for the relationship between △PSQI score and △HbA1c in men was greater than that in women, and for age was ß61-75years < ß46-60years < ß30-45years. The strongest relationship between △PSQI and △HbA1c was in men aged 30-45 years (ß = 0.452, P < 0.01). Subjective sleep disturbance among people with diabetes was not related to glycaemic status in the whole sample, but there was a correlation in women. The change in subjective sleep disturbance correlated with the change in glycaemia, most strongly in younger participants, especially men aged 30-45 years.

Platelet-endothelial cell interactions modulate smooth muscle cell phenotype in an in vitro model of type 2 diabetes mellitus.

Platelet (PLT)-endothelial cell (EC) interaction appears to contribute to phenotypic transition of vascular smooth muscle cells (VSMCs), which play an important role in the physiological and pathological process of vascular complications in type 2 diabetes mellitus (DM2). However, the precise mechanisms by which interactions between PLTs and ECs affect VSMC phenotype have largely remained unclear. We determined the effect of diabetic PLT-EC interaction to influence VSMC migration, proliferation, and phenotypic transformation in triple-cell coculture models using the quantitative real-time PCR, Western blot, fluorescence microscopy, wound scratch assays, CCK-8 assays, and gelatin zymography assays. Our results revealed DM2 PLT-EC interaction to be associated with a significant downregulation of VSMC-specific contractile phenotypic genes and proteins, including SM22α, smooth muscle actin, Smoothelin-B, and smooth muscle-myosin heavy chain. Inversely, VSMC-specific proliferative phenotype gene and protein levels, including cyclin D1 and 2, nonmuscle myosin heavy chain B, and PCNA were in upregulation. Furthermore, the DM2-originated PLT-EC interaction promoted the expression level of transforming growth factor-ß1, and the PI3K/Akt and matrix metalloproteinase 9 signaling pathway was activated subsequently. Finally, these reactions contributed to a synthetic phenotype of VSMCs, including the proliferation, migration, and gelatinolytic activities. These findings suggest that PLT-EC interaction modulates the phenotypic transition of VSMCs between a contractile and proliferative/synthetic phenotype under diabetic conditions, conceivably providing important implications regarding the mechanisms controlling the VSMC phenotypic transition and the development of cardiovascular complications.

The prevalence of alcohol dependence and its association with hypertension: a population-based cross-sectional study4 in Xuzhou city, China.

BACKGROUND: To describe the prevalence of alcohol dependence and to explore the relationship between alcohol dependence and newly detected hypertension in China. METHODS: A multistage stratified cluster sampling method was used to obtain samples from February to June 2013. The Michigan Alcoholism Screening Test was used to estimate alcohol dependence level. A standard questionnaire measured other independent variables. Enumeration data were analyzed using chi-square; quantitative data were analyzed using t-tests. Spearman correlation analysis and multivariate logistic regression analysis were performed to identify the relationship between alcohol dependence and hypertension. RESULTS: The alcohol dependence rate was 11.56%; 22.02% of males (3854/17501) and 1.74% of females (324/18656) were classified as alcohol dependent. The newly detected hypertension rate was 9.46% (3422/36157). Significant associations were found between alcohol dependence levels and blood pressure (P < 0.01). Alcohol dependence was positively correlated with systolic blood pressure (r = 0.071, P < 0.01) and diastolic blood pressure (r = 0.077, P < 0.01) and was an independent risk factor for hypertension after adjusting for confounders (low alcohol dependence: odds ratio [OR] = 1.44, 95% confidence intervals [CI] = 1.14-1.81, P < 0.01; light alcohol dependence: OR = 1.35, 95% CI = 1.11-1.64, P < 0.01; medium alcohol dependence: OR = 1.83, 95% CI = 1.40-2.41, P < 0.01). CONCLUSION: Alcohol dependence was high and associated with hypertension. Health education and precautions against alcoholism should be implemented in Xuzhou city.

The heterogeneity of islet autoantibodies and the progression of islet failure in type 1 diabetic patients.

Type 1 diabetes mellitus is heterogeneous in many facets. The patients suffered from type 1 diabetes present several levels of islet function as well as variable number and type of islet-specific autoantibodies. This study was to investigate prevalence and heterogeneity of the islet autoantibodies and clinical phenotypes of type 1 diabetes mellitus; and also discussed the process of islet failure and its risk factors in Chinese type 1 diabetic patients. A total of 1,291 type 1 diabetic patients were enrolled in this study. Demographic information was collected. Laboratory tests including mixed-meal tolerance test, human leukocyte antigen alleles, hemoglobinA1c, lipids, thyroid function and islet autoantibodies were conducted. The frequency of islet-specific autoantibody in newly diagnosed T1DM patients (duration shorter than half year) was 73% in East China. According to binary logistic regressions, autoantibody positivity, longer duration and lower Body Mass Index were the risk factors of islet failure. As the disease developed, autoantibodies against glutamic acid decarboxylase declined as well as the other two autoantibodies against zinc transporter 8 and islet antigen 2. The decrease of autoantibodies was positively correlated with aggressive beta cell destruction. Autoantibodies can facilitate the identification of classic T1DM from other subtypes and predict the progression of islet failure. As there were obvious heterogeneity in autoantibodies and clinical manifestation in different phenotypes of the disease, we should take more factors into consideration when identifying type 1 diabetes mellitus.