Weiping Jia

Shanghai University, Shanghai, Shanghai Shi, China

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Publications (253)1157.63 Total impact

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    ABSTRACT: To explore the factors mediating the relationship between body mass index (BMI) and diabetic retinopathy (DR) in Chinese type 2 diabetes patients. This is a cross-sectional study. Data of 2,533 patients with type 2 diabetes were studied from the Shanghai Diabetes Registry Database. DR was assessed using non-mydriatic fundus photography and graded as non-DR, mild-moderate (DR I-II), and sight-threatening (DR III-IV). BMI (kg/m(2)) was classified as normal weight (18.5 ≤ BMI < 25), overweight (25 ≤ BMI < 30), and obese (BMI ≥ 30). β cell function was evaluated by fasting C-peptide (FCP). DR was present in 701 (27.7 %) patients. Patients with DR had lower BMI (24.3 vs. 24.9 kg/m(2), P = 0.001) and fasting C-peptide (1.46 vs. 1.86 ng/ml, P < 0.001) than those without DR. The association between BMI (2 kg/m(2) interval) and DR was U-shaped; patients with BMI 28-29.9 kg/m(2) had the lowest DR rate. Compared with normal weight, overweight was associated with reduced risk of any DR [odds ratio (OR) 0.73], DR I-II (OR 0.76), and DR III-IV (OR 0.64) after adjustment for sex, age at diabetes diagnosis, and duration of diabetes. This negative association attenuated after adjustment for other confounders and became nonsignificant after further adjustment for FCP. Patients with different BMI categories had similar DR risk when stratified by FCP tertiles. Overweight patients have lower DR prevalence than normal weight individuals, which may be attributable to better β cell function in overweight patients.
    Acta diabetologica. 01/2015;
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    ABSTRACT: Background and Objectives This study aimed to investigate how the organic cation transporter 2 nucleotide polymorphism at site 808 (G → T) affects metformin pharmacokinetics and its long-term anti-diabetic effect. Methods A total of 220 newly diagnosed type 2 diabetes patients taking oral metformin were recruited, genotyped and then divided into three groups by SLC22A2 genotypes (G/G, G/T, T/T). Nine patients in the GG genotype group, five patients in the GT genotype group and four patients in the TT genotype group were randomly selected for the metformin pharmacokinetic study. A randomized cohort study with 1-year follow-up was performed to clarify the metformin pharmacodynamics. Results After 1 year, the decrease in glycosylated hemoglobin (HbA1c) levels in subjects with the heterozygous variant genotype (GT) was significantly greater than in those with the wild-type homozygote (−2.2 % in GT vs. −1.1 % in GG, P 1c levels, exercise and diet in each group. There were also differences in the pharmacokinetic parameters (95 % confidence interval) of metformin between these two groups [area under the concentration–time curve (AUC)0–∞ 19.7 (15.7–23.8) vs. 14.3 (11.7–16.9) μg h/L; renal clearance (CLr) 16.8 (8.5–25.0) vs. 34.1 (24.9–43.2) L/h; tubular secretion clearance (CLt) 8.1 (2.2–18.1) vs. 22.7 (15.5–29.8) L/h; all P P Conclusion As well as gender, the glucose-lowering efficiency of metformin can be enhanced by SLC22A2 808G > T variants through the delay of its transportation and CLr in Chinese type 2 diabetes populations.
    Molecular Diagnosis & Therapy 01/2015; · 2.59 Impact Factor
  • Miao Chen, Cheng Hu, Weiping Jia
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    ABSTRACT: Glinides, including repaglinide, nateglinide and mitiglinide, are a type of fasting insulin secretagogue that could help to mimic early-phase insulin release, thus providing improved control of the postprandial glucose levels. Glinides stimulate insulin secretion by inhibiting ATP-sensitive potassium channels in the pancreatic β-cell membrane. Although glinides have been widely used clinically and display excellent safety and efficacy, the response to glinides varies among individuals, which is partially due to genetic factors involved in drug absorption, distribution, metabolism and targeting. Several pharmacogenomic studies have demonstrated that variants of genes involved in the pharmacokinetics or pharmacodynamics of glinides are associated with the drug response. Polymorphisms of genes involved in drug metabolism, such as CYP2C9, CYP2C8 and SLCO1B1, may influence the efficacy of glinides and the incidence of adverse effects. In addition, Type 2 diabetes mellitus susceptibility genes, such as KCNQ1, PAX4 and BETA2, also influence the efficacy of glinides. In this article, we review and discuss current pharmacogenomics researches on glinides, and hopefully provide useful data and proof for clinical application.
    Pharmacogenomics 01/2015; 16(1):45-60. · 3.43 Impact Factor
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    ABSTRACT: Abstract Background: This study was designed to clarify the influence of metformin on serum carbohydrate antigen 199 (CA199) levels and its associated factors in Chinese type 2 diabetes mellitus (T2DM) patients. Subjects and Methods: In total, 1,253 T2DM patients were enrolled, including a non-metformin group (n=616), a short-term metformin group (at least 1 week to 2 years; n=325), and a long-term metformin group (≥2 years; n=312). Their clinical and biochemical characteristics were collected and compared. After 1 year, the biochemical parameters were re-examined in 296 patients. Sex hormones were determined, and associations between CA199 and other variables were assessed. Results: At baseline, the incidence of abnormal CA199 levels was 14.7%, 8.9%, and 4.7% in the non-metformin, short-term metformin, and long-term metformin groups, respectively. CA199 levels in females were significantly higher than in males (P<0.01) and decreased significantly with the time of taking metformin (25.60±13.68 U/mL in non-metformin controls vs. 17.62±10.87 U/mL in the short-term group vs. 10.54±8.14 U/mL in the long-term group; P=0.000). The correlation and multiple stepwise regression analysis revealed that glycosylated hemoglobin, metformin, gender, total cholesterol, and follicle-stimulating hormone were independent impact factors on CA199 concentrations (all P<0.05). Binary logistic regression revealed that the risk of abnormal CA199 concentrations of the total population with short-term metformin or long-term metformin treatment decreased 11% (odds ratio=0.89; P=0.001) and 30% (odds ratio=0.70; P=0.000), respectively, at baseline. After a 1-year follow-up, the incidence of high CA199 level decreased in both the short-term and the long-term metformin group compared with that of controls (P<0.05). The extent of CA199 decrease in the long-term metformin group was the greatest (-17% vs. -4.9% in the short-term group vs. 3% in controls, P=0.000), and the group's risk of high blood CA199 level was reduced 67% (odds ratio=0.33; P=0.023). The reduction in women was more apparent than that in men (-18% vs. -5%, P=0.000). Conclusions: Metformin therapy reduced the CA199 level in Chinese T2DM patients, and its greatest decrease occurred in women with longer therapeutic time.
    Diabetes Technology &amp Therapeutics 12/2014; · 2.29 Impact Factor
  • Tao Wang, Weiping Jia, Cheng Hu
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    ABSTRACT: Obesity prevalence has increased in recent years. Lifestyle change fuels obesity, but genetic factors cause more than 50% of average variations in obesity. The advent of genome-wide association studies (GWAS) has hastened the progress of polygenic obesity research. As of this writing, more than 73 obesity susceptibility loci have been identified in ethnic groups through GWAS. The identified loci explain only 2% to 4% of obesity heritability, thereby indicating that a large proportion of loci remain undiscovered. Thus, the next step is to identify and confirm novel loci, which may exhibit smaller effects and lower allele frequencies than established loci. However, achieving these tasks has been difficult for researchers. GWAS help researchers discover the causal loci. Moreover, numerous biological studies have been performed on the polygenic effects on obesity, such as studies on fat mass- and obesity-associated gene (FTO), but the role of these polygenic effects in the mechanism of obesity remains unclear. Thus, obesity-causing variations should be identified, and insights into the biology of polygenic effects on obesity are needed.
    Frontiers of medicine. 12/2014;
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    ABSTRACT: To assess the associations between clinical characteristics and chronic complications in latent autoimmune diabetes in adults (LADA) and type 2 diabetes. This is a cross-sectional study. Our diabetes registry included 6,975 patients aged 30 to 75 years-old with phenotypic type 2 diabetes who underwent islet autoantibody screening between 2003 and 2012; 384 patients were identified to have LADA. Rates of chronic complications for LADA and type 2 diabetes were compared using a 1:2 matched design. Logistic models were fitted to identify the presence of diabetic chronic complications using clinical characteristics including gender, age, duration of diabetes, glycemic control and metabolic syndrome. When duration of diabetes <5 years, the prevalence of diabetic nephropathy (DN; 12.2% vs. 21.8%, P = 0.018) and diabetic retinopathy (DR; 8.1% vs. 15.9%, P = 0.011) were significantly lower in patients with LADA than patients with type 2 diabetes; the prevalence of DN and DR were comparable between both groups when duration ≥5 years. There was no significant difference in the prevalence of macrovascular complications between groups. The areas under the receiver operating characteristic curves (AUCs) based on the DN and DR models were larger for LADA than type 2 diabetes (0.72 vs. 0.61, P = 0.013; 0.76 vs. 0.68, P = 0.056). Patients with LADA had a lower prevalence of microvascular complications than patients with type 2 diabetes when the duration of diabetes was <5 years. Regression equation fitted by clinical characteristics can better predict the risk of microvascular complications in LADA than in type 2 diabetes. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Diabetes/Metabolism Research and Reviews 12/2014; · 3.59 Impact Factor
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    ABSTRACT: Obesity is associated with increased risk of developing numerous adverse health conditions. Cathepsin k (CTSK) is highly expressed in adipose tissues of obese patients and animal models. Although CTSK has been demonstrated to promote adipocyte differentiation in 3T3-L1 cells, the effects of CTSK selective inhibitor (CKSI) on weight gain and insulin resistance have not been well examined. High-fat diet (HFD) induced obese male C57BL/6 mice were fed a diet with or without CKSI for 8 weeks. The HFD induced increase in adipose tissue weight gain, increase in homeostasis model assessment (HOMA) index as well as accumulation of large adipocytes. After CKSI treatment, all these effects were blunted compared with the HFD control group. A study of the mechanism demonstrated a role for CKSI in significantly down-regulating the expression of two key transcription factors, peroxisome proliferators-activated receptor-γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα), which are markers of adipogenic differentiation. These results indicated that the CKSI possesses an anti-obesity effect, possibly involving the inhibition of adipocyte differentiation. CTSK is likely to be a new target of therapeutic intervention for the treatment of obesity.
    Endocrine Journal 11/2014; · 2.02 Impact Factor
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    ABSTRACT: It has been reported that obesity and serum low-density lipoprotein cholesterol (LDL-c) are important risk factors of cardiovascular disease (CVD). It is recognized that regionalized adiposity has different cardiovascular risk, visceral versus subcutaneous, is a better predictor of CVD. However, the relationship between regionalized adiposity and LDL-c is unclear. The present study was designed to investigate the relationship between visceral fat accumulation and serum LDL-c levels in a Chinese cohort.
    PLoS ONE 11/2014; 9(11):e112715. · 3.53 Impact Factor
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    ABSTRACT: To assess the involvement of peripheral nerve dysfunction in asymptomatic patients with latent autoimmune diabetes of adults (LADA) or type 2 diabetes (T2DM), and compare nerve conduction (NC) parameters between the two groups. A total of 1635 patients without symptoms and signs relevant to diabetic polyneuropathy (1275 with T2DM and 360 with LADA) were included and were further categorized into 3 groups according to diabetes duration: <5years, 5-14years and ≥15years. All subjects underwent nerve conduction studies. Abnormal NC was defined as the abnormality of NC parameters in two or more anatomical nerves. In both LADA and T2DM patients, the proportions of abnormal NC increased significantly with increasing durations (both P for trend <0.001). Specifically, abnormal NC was present in 18.5%, 38.8% and 66.7% of LADA patients with duration of <5years, 5-14years and ≥15years, respectively. Those numbers were 24.8% (P=0.152, vs. LADA), 25.3% (P=0.023, vs. LADA) and 62.8% (P=0.723, vs. LADA) in T2DM. Regarding NC parameters, T2DM patients had higher composite Z-scores of latency than LADA patients within 5years of duration (P=0.001). In patients with duration of 5-14years, the latency Z-scores were comparable between the two groups (P=0.164), whereas the Z-scores of amplitude were lower (the lower the worse) in LADA than in T2DM (P=0.035). Peripheral nerve dysfunction is common in asymptomatic patients with LADA or T2DM. Findings of the study suggest that LADA and T2DM differ in the pattern of peripheral nerve involvement over diabetes duration. Copyright © 2014 Elsevier Inc. All rights reserved.
    Journal of Diabetes and its Complications 11/2014; · 1.93 Impact Factor
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    ABSTRACT: To investigate the impact of common variants of FNDC5 on type 2 diabetes and clinical traits related to glucose metabolism in a large Chinese population sample.
    PLoS ONE 11/2014; 9(11):e109957. · 3.53 Impact Factor
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    ABSTRACT: Aims To assess the predictive value of glycated albumin (GA) and other risk factors on a progression of diabetic retinopathy (DR). Methods In this retrospective longitudinal study, we enrolled the subjects with type 2 diabetes who had undergone fundus photography twice with 5 years apart between January 2006 and December 2012, and been measured consecutively for hemoglobin A1c (HbA1c) and GA levels every 3 or 6 months. The subjects were divided into two groups with or without a progression of DR. The mean HbA1c and mean GA were calculated separately by the sum of all measured values divided by the numbers of values throughout the study period. Results Of the 359 subjects, progression group showed significantly higher diabetes duration (8.41 ± 5.72 vs. 6.46 ± 5.77, P < 0.01), baseline HbA1c (9.13 ± 2.71 vs. 8.41 ± 2.32, P < 0.05), fasting plasma glucose (8.71 ± 2.78 vs. 7.94 ± 2.63, P < 0.05), 2 h-postprandial glucose (15.12 ± 11.20 vs.13.14 ± 4.72, P < 0.05), eGFR (114.81 ± 39.15 vs. 103.23 ± 32.18, P < 0.01), mean HbA1c (8.32 ± 1.69 vs. 7.39 ± 1.35, P < 0.01) and mean GA (22.66 ± 5.92 vs. 19.83 ± 5.18, P < 0.01) than non-progression group. The frequencies of subjects with DR progression increased obviously with the increment of baseline HbA1c, mean HbA1c and mean GA according to quartile stratification of the above three glucose parameters. Multivariable binary logistic regression analysis investigated that the factors affected the DR progression were the presence of DR at baseline (OR = 0.391, P = 0.005), mean HbA1c (OR = 1.389, P = 0.021), mean GA (OR = 1.087, P = 0.039) and eGFR (OR = 1.008, P = 0.045). The optimal cut-off values of mean HbA1c and GA to predict DR progression were 7.27% and 21.85%, respectively. Conclusions The presence of DR at baseline, poor glycemic control, glycated albumin, and impaired renal function predicted DR progression in patients with type 2 diabetes.
    Journal of Diabetes and its Complications 11/2014; · 1.93 Impact Factor
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    ABSTRACT: The aim of this study was to investigate the association between serum vitamin D levels and visceral adipose as well as with nonalcoholic fatty liver disease (NAFLD) in Chinese postmenopausal women. Four hundred and fifty-one postmenopausal women from 45 to 74 years of age (mean: 57.3±4.6) were enrolled. All subjects participated in the Shanghai Obesity Study between June and August 2011 and received abdominal magnetic resonance imaging scans and an abdominal ultrasonography examination. Patients with a visceral fat area (VFA) ≥80 cm2 were classified as abdominally obese. Serum 25-hydroxyvitamin D3 (25(OH)D3) levels were measured with an electrochemiluminescence immunoassay. The prevalence of NAFLD in this study population was 34.81% (n=157). Compared with the non-abdominal obesity group, the abdominal obesity group showed significantly lower serum 25(OH)D3 levels (11.23 [8.64-14.12] ng/mL vs. 12.56 [9.41-15.98] ng/mL; P<0.01). Regardless of the abdominal obesity status, serum 25(OH)D3 levels in the NAFLD subgroups were lower than the non-NAFLD subgroups (non-abdominal obesity group: 11.14 [8.63-13.81] ng/mL vs. 12.92 [9.48-16.37] ng/mL, P<0.05; abdominal obesity group: 10.86 [8.61-13.56] ng/mL vs. 11.55 [8.82-16.38] ng/mL, P<0.05). Partial correlation analyses demonstrated a negative correlation of serum 25(OH)D3 levels with VFA (P<0.05). Logistic regression analysis showed high serum 25(OH)D3 levels were a protective factor for NAFLD after adjusting for risk factors such as VFA. In conclusion, independent of visceral obesity, vitamin D is inversely correlated with NAFLD in Chinese postmenopausal women.This article is protected by copyright. All rights reserved.
    Clinical and Experimental Pharmacology and Physiology 11/2014; · 2.41 Impact Factor
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    ABSTRACT: This study aimed to assess the effects of active and passive smoking on chronic kidney disease (CKD) in patients with type 2 diabetes mellitus (T2DM). Seven hundred and five patients with T2DM were recruited in the study and were divided into three groups based on smoking status as active smokers, passive smokers and non-smokers. Twenty-four hour urinary albumin excretion (24hUAE) was measured, and estimate glomerular filtration rate (eGFR) was calculated with age and blood creatinine levels. (1)The proportion of CKD in T2DM in the present study was 31.63% (223/705) with 28.6% (22/77) , 30.0% (15/50) and 29.6% (73/247) for non-smokers, passive smokers and active smokers in men, and 29.9% (40/134), 35.9% (66/184) and 7/13 for non-smokers, passive smokers and active smokers in women, respectively. In comparison with non-smokers, a higher risk of CKD was found in both passive and active smokers (OR = 1.07 and OR = 1.05 in men; OR = 1.31 and OR = 2.74 in women, respectively). (2) Compared with non-smokers, passive smokers had a significant higher risk for albuminuria in women (OR = 2.02, P = 0.016) . (3) After adjusting for gender, age, duration of T2DM, BMI, systolic blood pressure, glycosylated hemoglobin A1C and lipids, there was a significant decrease in eGFR between active and never smokers (P = 0.018) or passive smokers (P = 0.000) in women. No differences could be found in eGFR between each smoking statues in men. Smoking exposure alone confers a high risk for CKD in patients with T2DM. Our results highlight an importance in implementation of a smoke-free environment for patients with T2DM.
    Zhonghua nei ke za zhi. 11/2014; 53(11):858-64.
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    ABSTRACT: Background: Fibroblast growth factor 21 (FGF21) is a hormone involved in the metabolism of carbohydrates and lipids. Increased circulating FGF21 levels are closely associated with nonalcoholic fatty liver disease (NAFLD). However, the association between genetic variations of FGF21 and NAFLD remains unknown. In our study, we aimed to investigate the association of these genetic variations with serum FGF21 levels and NAFLD. Methods: We genotyped four single nucleotide polymorphisms (SNPs) in FGF21 and its flanking region in 340 nondiabetic subjects. NAFLD was defined as the presence of a specific abdominal ultrasonographic pattern. Serum FGF21 concentrations were measured using an enzyme-linked immunosorbent assay kit. Results: We found significant evidence of an association with NAFLD for rs499765 (p = 0.039). After adjusting for age and sex, the effect of rs499765 on NAFLD remained significant (p = 0.045). However, after adjusting for multiple comparisons, no association was found. Moreover, rs499765 was associated with serum FGF21 levels (p = 0.030). In addition, both rs2071699 and rs838136 showed an association with serum aspartate aminotransferase levels (p = 0.049 and p = 0.047, respectively). The SNP rs838136 also showed a correlation with serum alanine aminotransferase concentrations after adjustment for body mass index (p = 0.034). We also combined the minor group with the heterozygous genotype and observed that rs499765 had an effect on FGF21 (p = 0.031). Conclusion: The variant rs499765 adjacent to FGF21 is associated with serum FGF21 levels and NAFLD in a Chinese nondiabetic population. © 2014 S. Karger AG, Basel.
    Journal of Nutrigenetics and Nutrigenomics 10/2014; 7(3):121-129. · 1.31 Impact Factor
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    ABSTRACT: Background & Aims As the main detoxifying organ of the body, the liver possesses a remarkable ability to regenerate after toxic injury, tissue resection or viral infection. A growing number of cellular signaling pathways have been implicated in orchestrating the process of liver regeneration. Here we investigated the role of inositol-requiring enzyme-1α (IRE1 α), a key signal transducer of the unfolded protein response (UPR), in liver regeneration. Methods Utilizing mice with hepatocyte-specific deletion of IRE1 α, we examined the role of IRE1 α in liver regeneration after challenges with carbon tetrachloride (CCl4) or hepatic surgery. We also investigated if IRE1 α deficiency could affect the activation state of signal transducer and activator of transcription 3 (STAT3) in hepatocytes. Using co-immunoprecipitation and glutathione S-transferase (GST) pull-down assays, we analyzed whether IRE1 α could interact with STAT3 to regulate its phosphorylation. Results We found that in response to CCl4-induced liver damage or after two thirds partial hepatectomy (PH), abrogation of IRE1 α caused marked exacerbation of liver injury and impairment in regenerative proliferation of hepatocytes in mice. Furthermore, IRE1 α deficiency resulted in dampened STAT3 activation, and restoration of IRE1 α expression led to sustained phosphorylation of STAT3 in IRE1 α -null hepatocytes. Additionally, IRE1 α could directly and constitutively associate with STAT3, leading to elevated phosphorylation when stimulated by IL-6. Conclusions These results suggest that IRE1 α may promote liver regeneration through acting as a signaling platform to regulate the STAT3 pathway.
    Journal of Hepatology 10/2014; · 10.40 Impact Factor
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    ABSTRACT: The present study was designed to determine the prevalence of 'metabolically healthy but obese' (MHO) and 'metabolically abnormal but not obese' (MANO) phenotypes in Chinese population, and to investigate the association of these two phenotypes with the risk of diabetes and cardiovascular disease (CVD). A total of 2,764 subjects aged 30-90 were followed up over a mean period of 43.80 ± 11.25 months. The metabolic syndrome was defined according to the joint committee for developing Chinese guidelines on prevention and treatment of dyslipidemia in adults. Subjects with body fat percentage (BF %) >25 % for men or BF % >35 % for women were defined as being obese. The proportion of MHO and MANO phenotypes were 22.9, 7.6 % in men, and 26.2, 6.0 % in women, respectively. The MANO phenotype was associated with increased risk for diabetes both in men [hazard ratios (HR): 4.44 (1.21-16.26)] and women [HR: 8.68 (2.87-24.96)] after adjustment of age, serum total cholesterol (TC), triglycerides (TG), and family history of diabetes. This association held for CVD in women [HR: 2.87 (1.44-5.73)], but not in men after adjustment of age, serum TC, TG, and family history of CVD. No association was observed between the MHO phenotype and incident diabetes or CVD. MHO and MANO phenotypes are common in Chinese population. Metabolic risk factors appeared to play a more important role in the development of diabetes and CVD than body fat alone.
    Endocrine 10/2014; · 3.53 Impact Factor
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    ABSTRACT: BackgroundsWe hypothesize that depression in type 2 diabetes might be associated with poor glycemic control, in part due to suboptimalself-care. We tested this hypothesis by examining the associations of depression with clinical and laboratory findingsin a multicenter survey of Chinese type 2 diabetic patients.Method2538 patients aged 18-75 yearsattending hospital-based clinics in fourcities in China underwent detailed clinical-psychological-behavioral assessment during a 12-month periodbetween 2011 and 2012. Depression was diagnosed if Patient Health Questionnaire-9(PHQ-9) score≥10.Diabetes self-care and medication adherence were assessed using the Summary of Diabetes Self-care Activities and the 4-item Morisky medication adherence scale respectively.ResultsIn this cross-sectional study (mean age: 56.4±10.5[SD] years, 53% men), 6.1%(n=155) had depression. After controlling for study sites, patients with depression had higher HbA1c(7.9±2.0vs. 7.7±2.0%, P=0.008) and were less likely to achieve HbA1c goal of <7.0%(36.2% vs. 45.6%, P=0.004)than those without depression. They were more likely to report hypoglycemia and to have fewer days ofbeing adherent to their recommended diet, exercise, foot care and medication. In logistic regression, apart from young age, poor education, long disease duration, tobacco use,high body mass index,use of insulin, depression was independently associated with failure to attain HbA1c target(Odds Ratio[OR]=1.56, P=0.028). The association between depression and glycemic control became non-significant after inclusion of adherence to diet, exerciseand medication(OR=1.48, P=0.058).Conclusion Depression in type 2 diabetes was closely associated with hyperglycemiaandhypoglycemia which might be partly mediated through poor treatment adherence.
    Journal of Diabetes 10/2014; · 2.94 Impact Factor
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    ABSTRACT: Adipose tissue inflammation and perturbation of adipokine secretion may contribute to the pathogenesis of cardiovascular diseases (CVD). Lipocalin-2 (LCN2), mainly released from adipocytes, has been shown to be positively associated with CVD in cross-sectional studies. We aimed to evaluate the association of LCN2 with CVD involving a population-based cohort recruited from the Shanghai Diabetes Study.
    Arteriosclerosis Thrombosis and Vascular Biology 09/2014; · 5.53 Impact Factor
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    ABSTRACT: Fasting plasma glucose (FPG) has been recognized as an important indicator for the overall glycemic state preceding the onset of metabolic diseases. Most genome-wide association loci for FPG so far been identified were derived from populations with European ancestry with a few exceptions. To extend a thorough catalog for FPG loci, we conducted meta-analyses of 13 genome-wide association studies in up to 24,740 non-diabetic subjects with East Asian ancestry. Follow-up replication analyses in up to additional 21,345 participants identified three new FPG loci reaching genome-wide significance in or near PDK1-RAPGEF4, KANK1 and IGF1R. Our results could provide additional insight into the genetic variation implicated in fasting glucose regulation.
    Diabetes 09/2014; · 7.90 Impact Factor
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    ABSTRACT: Abstract Objective: Serum cystatin C is a sensitive marker of kidney function and recent studies have shown that cystatin C plays a critical role in degenerative diseases of both central and peripheral nervous systems. The aim of this study was to explore the relationship between serum cystatin C and diabetic peripheral neuropathy (DPN) in type 2 diabetes. Methods: Totally 937 type 2 diabetic patients were enrolled in this cross-sectional study. Serum cystatin C concentration was measured with immunoturbidimetry. DPN was evaluated by neurological symptoms, neurological signs, neurothesiometer and electromyogram. Results: Serum cystatin C levels were significantly higher in DPN patients [1.3(1.1-1.5)mg/L] compared with signs of DPN[1.1(0.9-1.3)mg/L, p<0.001] and non-DPN patients (1.0(0.9-1.3)mg/L, p<0.001). Multiple regression analysis revealed that DPN was associated with age, diabetes duration, glycosylated hemoglobin A1c(HbA1c) and serum cystatin C. Spearman correlation analysis showed that serum CysC was closely related to age, sex, diabetes duration, hypertension, glomerular infiltration rate and serum creatinine. Patients were divided into quartiles according to the serum cystatin C levels. Compared with Quartile1(referent), the risk of DPN was significantly higher in Quartile2(OR, 1.753; 95%CI 1.055-2.912; p<0.05), Quartile3(OR, 2.463; 95%CI 1.445-4.917; p<0.01) and Quartile4(OR, 5.867; 95%CI 2.075-16.589; p<0.01). Receiver operating characteristic analysis revealed that the optimal cutoff point of serum cystatin C to indicate DPN was 1.25mg/L in male patients and 1.05mg/L in female patients. And high serum cystatin C indicated double risk of DPN. Conclusions: High serum cystatin C is closely associated with DPN and may be a potential biomarker for DPN in type 2 diabetes.
    European Journal of Endocrinology 09/2014; · 3.69 Impact Factor

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Institutions

  • 2014
    • Shanghai University
      Shanghai, Shanghai Shi, China
  • 2008–2014
    • Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine
      Shanghai, Shanghai Shi, China
  • 2007–2014
    • Shanghai Clinical Research Center
      Shanghai, Shanghai Shi, China
  • 2006–2014
    • Shanghai Jiao Tong University
      • • School of Pharmacy
      • • Department of Pediatrics (Sixth People's Hospital)
      Shanghai, Shanghai Shi, China
  • 2013
    • Henan Provincial People’s Hospital
      Cheng, Henan Sheng, China
    • The Chinese University of Hong Kong
      • Department of Paediatrics
      Hong Kong, Hong Kong
    • China-Japan Friendship Hospital
      Peping, Beijing, China
  • 2002–2013
    • Shanghai Cancer Institute
      Shanghai, Shanghai Shi, China
  • 2012
    • Soochow University (PRC)
      Wu-hsien, Jiangsu Sheng, China
    • Shanghai University of Traditional Chinese Medicine
      Shanghai, Shanghai Shi, China
    • The University of Hong Kong
      • Department of Medicine
      Hong Kong, Hong Kong
  • 2010
    • Shanghai Putuo District People's Hospital
      Shanghai, Shanghai Shi, China
  • 2006–2009
    • University of Oxford
      • • Wellcome Trust Centre for Human Genetics
      • • Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM)
      Oxford, ENG, United Kingdom