ObjectiveWe aimed to investigate whether elevated serum uric acid concentrations are associated with higher risk of metabolic syndrome (MetS) and carotid atherosclerosis in patients with type 2 diabetes.MethodsWe conducted a population-based cross-sectional survey in Shanghai, with a total of 395 men and 631 women age 41 to 92 years. The carotid artery intima-media thickness (IMT) and carotid atherosclerotic plaques (PLQ) were measured by B-mode ultrasound. MetS was defined according to the updated National Cholesterol Education Program Adult Treatment Panel III criteria for Asian Americans.ResultsUric acid levels were negatively associated with duration of diabetes, fasting plasma glucose, glycohemoglobin, eGFR, HDL-cholesterol (all P < 0.001) and positively with BMI, CRP, waist circumference, triglycerides, systolic blood pressure, ACR, HOMA-IR and IMT (all P < 0.05). In the highest quartile of uric acid levels, the risks were substantially higher for MetS [odds ratio 3.97, (95% confidence interval 2.58-6.13)] (P < 0.001 for trend) and PLQ [odds ratio 2.71 (95% confidence interval 1.62-4.47)] (p = 0.013 for trend) compared with that in the lowest quartile of uric acid levels after multiple adjustment. These associations remained significant after further adjustment for potential confounders.ConclusionsSerum uric acid level is associated with MetS and is an independent risk factor for carotid atherosclerosis in patients with type 2 diabetes.

BackgroundLipocalin-2 is a novel adipokine with connection to insulin resistance. In this study, we aimed to investigate the association of serum lipocalin-2 with glucose metabolism and other metabolic phenotype in a large-scale Chinese population.MethodsWe evaluated serum lipocalin-2 in a cross-sectional sample of 2519 Chinese aged from 50 to 82 year in a Shanghai downtown district by ELISA. Glucose, insulin, lipid profile, inflammatory markers, and adipokines were also measured.ResultsSerum lipocalin-2 was significantly higher in subjects with isolated impaired fasting glucose, isolated impaired glucose tolerance, combined impaired fasting glucose/impaired glucose tolerance and newly-diagnosed type 2 diabetes than in those with normal glucose regulation. Lipocalin-2 elevation was clearly associated with a higher risk for impaired glucose regulation (OR 1.30 for each 10 ng/ml increase in serum lipocalin-2, 95% CI 1.23-1.62, p = 0.009) after adjustment of age, gender, smoking, alcohol drinking, family history of diabetes, serum CRP, serum adiponectin, serum CXCL5, HOMA-IR, BMI, and waist/hip ratio. The OR for participants with impaired glucose regulation and type 2 diabetes was 1.31 (95% CI 1.21-1.69, p < 0.001).ConclusionsOur findings suggest that elevated serum lipocalin-2 is closely and independently associated with impaired glucose regulation and type 2 diabetes.

BackgroundLow socioeconomic status (SES) is associated with adverse cardiovascular risk factor patterns and poor outcomes in patients with diabetes. The aim of this study was to determine whether SES is associated with the control of blood glucose, blood pressure, blood cholesterol (3Bs), and diabetic complications in Chinese adults with type 2 diabetes.MethodsData regarding patients’ demographics, social economics, diabetes complications, and cardiovascular risk profiles were analyzed for 25,454 patients. The outcomes of interest were the proportions of patients with HbA1c <7.0 %, blood pressure <140/80 mmHg, total serum cholesterol <4.5 mmol/L, and diabetes complications. Multivariable logistic regression was used for analysis.ResultsOf the 25,454 patients, the least educated patients (1695, 6.7 %) had the highest chances of developing cardiovascular diseases (p = 0.048), cerebrovascular diseases (p < 0.001), and retinopathy (p < 0.001). The patients with lowest household income (10,039, 40.8 %) had the highest prevalence of retinopathy (p < 0.001) and neuropathy (p < 0.001). The most educated patients were more likely than the least educated patients to achieve HbA1c <7.0 % [adjusted odds ratio (OR) 1.38; 95 % confidence interval (95 % CI) 1.22–1.56] and 3B goals (adjusted OR 1.30; 95 % CI 1.11–1.53). The patients with highest household income were more likely to achieve BP < 140/80 mmHg (adjusted OR 1.16; 95 % CI 1.07–1.27), but less likely to reach HbA1c < 7.0 % (adjusted OR 0.90; 95 % CI 0.83–0.98) than those lowest income patients.ConclusionsLow SES was associated with poor metabolic control and more diabetes complications in adult patients in China. Individual diabetes management based on the SES of patients is encouraged.Electronic supplementary materialThe online version of this article (doi:10.1186/s12933-016-0376-7) contains supplementary material, which is available to authorized users.

Recent genome-wide association studies reported that GCKR rs780094 polymorphism is associated with elevated fasting serum triglyceride levels and elevated levels of C-reactive protein (CRP). There are a ample of data on the association between circulating triglyceride, CRP concentrations and risk of non-alcoholic fatty liver (NAFLD). To determine whether the GCKR rs780094 polymorphism contributes to the development of non-alcoholic fatty liver, a case-control study was performed in 903 Chinese subjects. Among study population, 436 patients with B-mode ultrasound-proven NAFLD (318 with steatosis hepatis I°, 90 with steatosis hepatis II° and 28 with steatosis hepatis III°) and 467 controls were genotyped by using TaqMan allelic discrimination assays. We confirmed the association of GCKR rs780094 with NAFLD in Chinese people (OR = 1.607, 95% CI 1.139-2.271, P[dom] = 7.2 × 10(-3)). In this study, polymorphism in GCKR rs780094 was not significantly associated with the degree of fatty infiltration of the liver. In addition, the T-allele of GCKR rs780094 was significantly associated with increasing fasting triglyceride (P[add] = 3.8 × 10(-4)) and CRP (P[add] = 2.9 × 10(-4)) concentrations after adjusting for age, gender, and BMI. The association with NAFLD remained significant after adjustment for triglyceride, while adjustment for CRP abolished the association. Genetic variation in GCKR gene rs780094 polymorphism contributes to the risk of NAFLD in Chinese people. The effect of genotype on NAFLD is probably mediated through chronic low-grade systemic inflammation rather than through dislipidemia.

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Patients with diabetes having H. pylori infection demonstrated more gastrointestinal side effects than those without H. pylori infection after taking metformin. Furthermore, female gender, H. pylori infection, body mass index, triglycerides, age, and low-density lipoprotein-cholesterol are independent determinants of metformin's side effects.

Our data suggest that pre-existing non-symptomatic gastritis was associated with metformin-related gastrointestinal side effects.

Background Transcription factor 7-like 2 (TCF7L2), which previously known as TCF-4, is a major form of transcription factor involved in the downstream WNT signaling and exhibits the strongest association to diabetes susceptibility. Although we still do not know mechanistically how TCF7L2 exerts its physiological functions on pancreatic endocrine cells, it had been suggested that TCF7L2 may directly affect β-cell function by regulating the activation of PI3K/AKT signaling pathway. Methods MIN6 cells were transfected with TCF7L2 knockdown virus or lenti-TCF7L2 virus for 48 h to evaluate the contribution of TCF7L2 to the PI3K/AKT signaling pathway and pancreatic β-cell function. This was confirmed by measuring the expression of PI3K p85 and p-Akt by western blotting and insulin secretion by enzyme-linked immunosorbent assay (ELISA), respectively. Chromatin immunoprecipitation (ChIP) and polymerase chain reaction (PCR) experiments were performed to explore the genomic distribution of TCF7L2-binding sites in the promoter of PIK3R1, the affinity between which was analyzed by the luciferase reporter assay. Results In the present study, we strikingly identified that TCF7L2 could profoundly inhibit the expression of PIK3R1 gene and its encoding protein PI3K p85, which then could lead to the activation of PI3K/AKT signaling and stimulate insulin secretion in pancreatic β-cells. However, the integrity and stability of evolutionarily conserved TCF7L2-binding motif plays a very crucial role in the binding events between transcription factor TCF7L2 and its candidate target genes. We also found that the affinity of TCF7L2 to the promoter region of PIK3R1 alters upon the specific binding sites, which further provides statistical validation to the necessity of TCF7L2-binding motif. Conclusions This study demonstrated that TCF7L2 is closely bound to the specific binding regions of PIK3R1 promoter and prominently controls the transcription of its encoding protein p85, which further affects the activation of PI3K/AKT signaling pathway and insulin secretion.