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• The high FGF21 level and NAFLD were potential risk factor for MACE, respectively. • The association between FGF21 and MACE may be interacted by NAFLD. • Early screening and intervention for NAFLD are of great importance. We aimed to investigate whether there was a joint effect of fibroblast growth factor 21 (FGF21) and non-alcoholic fatty liver disease (NAFLD) or interaction on the incidence of cardiovascular diseases based on a community-dwelling population. Serum FGF21 levels were determined using an enzyme-linked immunosorbent method. NAFLD was diagnosed via ultrasonography. Multivariable-adjusted cox proportional hazards models were used to assess the joint effects of FGF21 and NAFLD on the major adverse cardiovascular events (MACE). A total of 1194 participants were enrolled in the final analysis. The multivariable-adjusted hazard ratio (HR) of MACE was 1.84 (95% confidence interval (CI) 1.18–2.86) in participants with diagnosed NAFLD at baseline, compared with those without NAFLD at baseline. The multivariable-adjusted HRs of MACE across quintiles of serum FGF21 levels at baseline were 1.00, 1.48 (95%CI 0.68–3.21), 2.01 (95%CI 0.98–4.13), 1.94 (95%CI 0.94–4.02) and 2.14 (95%CI 1.03–4.44) respectively. Participants with high FGF21 levels and NAFLD at baseline showed the highest risk of MACE with a significant interaction between the presence of NAFLD and serum FGF21 levels. Both FGF21 and NAFLD were associated with MACE, while the association between FGF21 and MACE may be interacted by the presence of NAFLD at baseline. [ABSTRACT FROM AUTHOR]

To develop a non-invasive assessment tool and compare it to other assessment tools among middle-aged and elderly Shanghainese, 15,309 individuals, who were 45-70 years old, not previously diagnosed with diabetes, and from a cross-sectional survey conducted between April 2013 and August 2014 in Shanghai, were selected into this study. The participants were randomly assigned to either the exploratory group or the validation group. Undiagnosed diabetes was defined according to the American Diabetes Association diagnostic criteria, and score points were generated according to the logistic regression coefficients. Age, family history of diabetes, hypertension, overweight/obesity, and central obesity all contributed to the constructed model, the Shanghai Nicheng diabetes screening score, with the area under the receiver-operating characteristic curve (AUC) being 0.654 (95% CI 0.637-0.670) in the exploratory group and 0.669 (95% CI 0.653-0.686) in the validation group. The score value of 6 was the optimal cut-point with the largest Youden's index. When applied to the validation group, our model had a similar discriminative ability to the New Chinese Diabetes Risk Score (AUC: 0.669 vs. 0.662, p = 0.187), and performed better than other screening scores for Chinese. However, our model was inferior to fasting plasma glucose, 2-hour plasma glucose, and glycosylated hemoglobin in detecting prevalent undiagnosed diabetes (AUC: 0.669 (0.653-0.686) vs. 0.881 (0.868-0.894), 0.934 (0.923-0.944), and 0.834 (0.819-0.848), all p < 0.001). Although non-invasive models, based on demographic and clinical information, are advisable in resource-scarce developing areas, regular blood glucose screening is still necessary among those aged 45 or older. [ABSTRACT FROM AUTHOR]

The lack of inhibitory control toward foods may cause unhealthy eating behavior and lead to obesity. However, previous research failed to reach consensus on the alterations in event-related potential (ERP) markers of inhibitory control, i.e., N2 and P3. We hypothesized that the ERP effects of inhibitory control reported in previous food-based Go/NoGo studies might be obscured by non-inhibitory processes associated with stimulus probability. We designed two food-based Go/NoGo tasks composed of stimuli with the same type and frequency of occurrence (60% non-foods, 20% high-calorie foods, 20% low-calorie foods), one with response inhibition toward high- and the other toward low-calorie foods. Such an experimental design allowed us to isolate neural activity associated with inhibitory control from that associated with non-inhibitory processes by constructing ERP difference waves between NoGo and Go trials with the same frequency of occurrence. Electroencephalography data were collected from 32 obese participants and 29 normal-weight controls. Obese participants showed significantly lower accuracy in NoGo trials than normal-weight controls in both tasks. ERP data suggested inhibition-related effects for P3 (P3d) but not N2 in the difference waves, and obese participants showed significantly decreased P3d amplitudes than normal-weight controls in both tasks. In addition, we found that across both groups, individuals with larger waist-to-hip ratios showed smaller P3d amplitudes in both tasks, while such correlations between body mass index and P3d amplitude were only observed in the high-calorie task. Our findings suggest that the decreased effect of P3, not N2, might reflect the neural substrate of inhibitory control deficits in obese people. Thus, P3 could serve as an important neural marker in the future development of new therapeutic strategy that aims to improve inhibitory control in obesity. [ABSTRACT FROM AUTHOR]

The lack of inhibitory control toward foods may cause unhealthy eating behavior and lead to obesity. However, previous research failed to reach consensus on the alterations in event-related potential (ERP) markers of inhibitory control, i.e., N2 and P3. We hypothesized that the ERP effects of inhibitory control reported in previous food-based Go/NoGo studies might be obscured by non-inhibitory processes associated with stimulus probability. We designed two food-based Go/NoGo tasks composed of stimuli with the same type and frequency of occurrence (60% non-foods, 20% high-calorie foods, 20% low-calorie foods), one with response inhibition toward high- and the other toward low-calorie foods. Such an experimental design allowed us to isolate neural activity associated with inhibitory control from that associated with non-inhibitory processes by constructing ERP difference waves between NoGo and Go trials with the same frequency of occurrence. Electroencephalography data were collected from 32 obese participants and 29 normal-weight controls. Obese participants showed significantly lower accuracy in NoGo trials than normal-weight controls in both tasks. ERP data suggested inhibition-related effects for P3 (P3d) but not N2 in the difference waves, and obese participants showed significantly decreased P3d amplitudes than normal-weight controls in both tasks. In addition, we found that across both groups, individuals with larger waist-to-hip ratios showed smaller P3d amplitudes in both tasks, while such correlations between body mass index and P3d amplitude were only observed in the high-calorie task. Our findings suggest that the decreased effect of P3, not N2, might reflect the neural substrate of inhibitory control deficits in obese people. Thus, P3 could serve as an important neural marker in the future development of new therapeutic strategy that aims to improve inhibitory control in obesity. [ABSTRACT FROM AUTHOR]

• Osteocalcin plays a protective role in insulin resistance and obesity. • Osteocalcin levels were independently and inversely correlated with prolonged QTc interval after adjusting for confounding factors among a community-based population. • VFA partially mediated the inverse correlation between osteocalcin levels and QTc interval. Osteocalcin, a bone-derived factor, could be a feasible marker for metabolic disorders and adverse cardiovascular outcomes. This study aimed to explore the correlation between serum osteocalcin levels and correct QT interval (QTc) interval prolongation, a risk factor of cardiac morbidity and mortality. We recruited 1210 subjects (age range: 26–80 years) in communities in Shanghai. Serum osteocalcin levels were determined using an electrochemiluminescence immunoassay. The QTc interval was measured using a 12-lead electrocardiogram and was calculated by the Bazett formula. A prolonged QTc interval was defined as QTc > 440 ms. Visceral fat area (VFA) was assessed by magnetic resonance imaging. A VFA of 80 cm2 was applied as a cut-off point for central obesity. Subjects with diabetes, overweight/obesity, or central obesity had significantly lower serum osteocalcin levels than those without (all P < 0.01). In subjects with a normal QTc interval, QTc interval lengthening accompanied decreasing osteocalcin levels (P for trend = 0.033), and the decline was more obvious in subjects with a prolonged QTc interval (P for trend = 0.022). Serum osteocalcin levels were correlated with the QTc interval (standardized β = –0.082, P = 0.005). Neither diabetes nor overweight/obesity was correlated with the QTc interval, whereas central obesity was positively correlated (P = 0.032). In addition, the correlation between osteocalcin levels and the QTc interval was attenuated when central obesity was included in the model simultaneously (standardized β = –0.075, P = 0.010). Mediation analysis revealed that VFA played a mediating role in the aforementioned correlation, and the estimated percentage of the total effect mediated by VFA was 20.9% (P = 0.007). VFA partially mediated the inverse correlation between the serum osteocalcin levels and QTc interval, suggesting that improving fat metabolism may be a mechanism by which osteocalcin protects against cardiovascular diseases. [ABSTRACT FROM AUTHOR]