The fatty liver index (FLI), which is an algorithm based on waist circumference, body mass index (BMI), triglyceride, and gamma-glutamyl-transferase (GGT), was initially developed to detect fatty liver in Western countries. Our study aimed to evaluate the accuracy and optimal cut-off point of the FLI for predicting nonalcoholic fatty liver disease (NAFLD) in middle-aged and elderly Chinese.This cross-sectional study included 8626 Chinese adults aged 40 years or above recruited from Jiading District, Shanghai, China. Anthropometric and biochemical features were collected by a standard protocol. NAFLD was diagnosed by hepatic ultrasonography. The accuracy and cut-off point of the FLI to detect NAFLD were evaluated by area under the receiver operator characteristic curve (AUROC) and the maximum Youden index analysis, respectively.The AUROC of the FLI for NAFLD was 0.834 (95% confidence interval: 0.825–0.842), and larger than that of its each individual component [0.786 (0.776–0.796), 0.783 (0.773–0.793), 0.727 (0.716–0.739), and 0.707 (0.695–0.719) for waist circumference, BMI, triglyceride, and GGT, respectively] (all P < .001). The optimal cut-off point of the FLI for diagnosing NAFLD was 30 with the maximum Youden Index of 0.51, achieving a high sensitivity of 79.89% and a specificity of 71.51%. The FLI-diagnosed NAFLD individuals were in worse metabolic characteristics (waist circumference, BMI, blood pressure, serum lipids, and aminotransferases) than ultrasonography-diagnosed NAFLD patients (all P < .05).The FLI could accurately identify NAFLD and the optimal cut-off point was 30 in middle-aged and elderly Chinese. As FLI-diagnosed NAFLD patients were in worse metabolism, much attention should be paid to the metabolic controls and managements of NAFLD.

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MHO was significantly associated with incident CKD, and the level of systemic inflammation partially explained this association.

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BackgroundMicroRNAs (miRNAs) have been shown to function in many different cellular processes, including proliferation, apoptosis, differentiation and development. miR-181a, -181b, -181c and -181d are miR-181 members of the family, which has been rarely studied, especially uveal melanoma.MethodsThe expression level of miR-181 family in human uveal melanoma cell lines was measured via real-time PCR (RT-PCR). The function of miR-181 on cell cycle was detected through Flow Cytometry assay. Microarray assay and Bioinformatics analysis were used to find the potential target of miR-181b, and dual-luciferase reporter assays further identified the target gene.ResultsMiR-181 family members were found to be highly homologous across different species and their upregulation significantly induces UM cell cycle progression. Of the family members, miR-181b was significantly overexpressed in UM tissues and most UM cells. Bioinformatics and dual luciferase reporter assay confirmed CTDSPL as a target of miR-181b. miR-181b over-expression inhibited CTDSPL expression, which in turn led to the phosphorylation of RB and an accumulation of the downstream cell cycle effector E2F1, promoting cell cycle progression in UM cells. Knockdown CTDSPL using siRNAs showing the same effect, including increase of E2F1 and the progression of cell cycle.ConclusionsMiR-181 family members are key negative regulators of CTDSPL-mediated cell cycle progression. These results highlight that miR-181 family members, especially miR-181b, may be useful in the development of miRNA-based therapies and may serve as novel diagnostic and therapeutic candidate for UM.Electronic supplementary materialThe online version of this article (10.1186/s13046-018-0679-5) contains supplementary material, which is available to authorized users.

Bile acid metabolism was reported to be involved in glucose metabolism homeostasis. However, the exact relationship between bile acid and glucose metabolism as well as insulin sensitivity is not clarified. Therefore, we sought to investigate the association between insulin sensitivity and hyperbileacidemia in type 2 diabetic and nondiabetic population.This community-based cross-sectional study included 9603 residents from Jiading, Shanghai, China, who were 40 years and older. Standardized questionnaire, anthropometric measurements and laboratory tests were conducted. Homeostasis model assessment of insulin resistance (HOMA-IR) ≥ 2.7 was defined as insulin resistance and fasting TBA ≥ 10 mmol/L was defined as hyperbileacidemia.Multivariate stepwise regression analysis revealed that HOMA-IR, age, and male sex were positively associated with hyperbileacidemia in both nondiabetic and diabetic participants. In multivariate logistic models, participants with insulin resistance had significantly higher risk of hyperbileacidemia compared to those who have no insulin resistance, in both nondiabetic and diabetic population (nondiabetic: OR = 1.76; 95% CI 1.42–2.19; P < 0.001; diabetic: OR = 1.56; 95% CI 1.06 – 2.31; P = 0.025, respectively). Further adjustment for the HbA1c level in diabetic population did not change the significant association (OR = 1.59; 95% CI 1.06 − 2.40; P = 0.024). In nondiabetic participants, each 1-unit increment of HOMA-IR conferred an 18% higher risk of hyperbileacidemia (95% CI 1.04–1.35; P = 0.013), whereas in diabetic participants, this association was similar but not significant (95% CI 0.95–1.59; P = 0.117).Insulin resistance was positively associated with hyperbileacidemia in both nondiabetic and diabetic population. The increase in the bile acid level in insulin-resistant population regardless of status of diabetes and glucose level indicated the important role of insulin resistance in the regulation of bile acid metabolism in human.

The T2D genetic susceptibility significantly modulated the association of BPA exposure with longitudinal increase in FPG levels.