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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]

• 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]