Kitaoka S.,Health Evaluation Center |
Ono K.,Kyoto University |
Nakano T.,National Hospital Organization Kyoto Medical Center |
Fujita M.,Kyoto University |
And 2 more authors.
Atherosclerosis | Year: 2010
Objective: Metabolic syndrome (MetS) is associated with impaired angiogenesis. Vascular endothelial growth factor (VEGF) plays a key role in angiogenesis through binding to its specific receptor, VEGF receptor-2 (VEGFR-2), whereas the expression of VEGF and VEGFR-2 in the myocardium of insulin-resistant rats is down-regulated. Soluble VEGF receptor-1 (sVEGFR-1) and -2 (sVEGFR-2) have been reported to inhibit angiogenesis both in vitro and in vivo. However, the balance between circulating levels of VEGF and its soluble receptors, which may reflect and/or affect cardiovascular VEGF signaling, in subjects with MetS is unknown. Methods and results: We carried out a cross-sectional study including 272 consecutive, apparently healthy subjects who were not receiving any drugs. Plasma levels of VEGF and serum levels of its soluble receptors were determined using enzyme-linked immunosorbent assays. VEGF and sVEGFR-1 levels did not differ between subjects with and those without MetS. However, sVEGFR-2 levels were significantly increased in MetS compared with non-MetS subjects. Stepwise regression analysis revealed that HOMA-IR was the strongest independent determinant of the sVEGFR-2 level. Accordingly, the mean sVEGFR-2 levels increased in proportion to both the accumulation of components of MetS and quartile of HOMA-IR. Interestingly, multiple regression analyses revealed that independent determinants of VEGF were the body mass index and blood pressure, whereas, in contrast, those of sVEGFR-2 were HOMA-IR and high-sensitivity C-reactive protein. Conclusions: The correlation of sVEGFR-2 with insulin resistance supports the need for further investigations to define the clinical utility and predictive value of serum sVEGFR-2 levels in cardiovascular dysfunction in MetS. © 2009 Elsevier Ireland Ltd. All rights reserved. Source
Liu C.-C.,Health Evaluation Center |
Liu C.-C.,Yuanpei University |
Wang S.-C.,National Tsing Hua University |
Kao C.-W.,GCRC Laboratory |
And 6 more authors.
Thrombosis and Haemostasis | Year: 2014
We investigated the role of activated B cells in thrombopoiesis through the production of interleukin (IL)-1beta and IL-6 in patients with essential thrombocythaemia. The number of B cells did not differ between essential thrombocythaemia patients, irrespective of the presence of Janus activated kinase-2 V617F mutation or wild type, and age-matched healthy adults. However, the number of IL-1beta/IL-6-producing B cells was significantly higher in essential thrombocythaemia patients than that in healthy controls. The relatively high level of IL-1beta/IL-6 production by B cells was associated with serum B cell-activating factor and expression of Toll-like receptor 4 on B cells. A high level of B cell-activating factor was present in essential thrombocythaemia patients with both Janus activated kinase-2 genotypes. Incubation with B cell-activating factor enhanced the expression of Toll-like receptor 4 on B cells. IL-1beta and IL-6 production was not stimulated by B cell-activating factor alone; Toll-like receptor 4 was activated by lipopolysaccharide or patients’ sera to produce IL-1beta and IL-6 in B cells. Moreover, essential thrombocythaemia patient B cells facilitated megakaryocyte differentiation when co-cultured with CD34+ haematopoietic stem cells. Antibody neutralisation of IL-1beta and IL-6 attenuated megakaryocyte differentiation. These data suggest that B cells play a crucial role in thrombopoiesis in essential thrombocythaemia patients. © Schattauer 2014. Source
Epicardial adipose tissue relating to anthropometrics, metabolic derangements and fatty liver disease independently contributes to serum high-sensitivity C-reactive protein beyond body fat composition: A study validated with computed tomography
Lai Y.-H.,Mackay Memorial Hospital |
Lai Y.-H.,Mackay Medicine Nursing and Management College |
Liu C.-C.,Health Evaluation Center |
Wu Y.-J.,Mackay Memorial Hospital |
And 15 more authors.
Journal of the American Society of Echocardiography | Year: 2012
Background: Epicardial adipose tissue (EAT) measured by echocardiography has been proposed to be associated with metabolic syndrome and increased cardiovascular risks. However, its independent association with fatty liver disease and systemic inflammation beyond clinical variables and body fat remains less well known. Methods: The relationships between EAT and various factors of metabolic derangement were retrospectively examined in consecutive 359 asymptomatic subjects (mean age, 51.6 years; 31% women) who participated in a cardiovascular health survey. Echocardiography-derived regional EAT thickness from parasternal long-axis and short-axis views was quantified. A subset of data from 178 randomly chosen participants were validated using 16-slice multidetector computed tomography. Body fat composition was evaluated using bioelectrical impedance from foot-to-foot measurements. Results: Increased EAT was associated with increased waist circumference, body weight, and body mass index (all P values for trend =.005). Graded increases in serum fasting glucose, insulin resistance, and alanine transaminase levels were observed across higher EAT tertiles as well as a graded decrease of high-density lipoprotein (all P values for trend <.05). The areas under the receiver operating characteristic curves for identifying metabolic syndrome and fatty liver disease were 0.8 and 0.77, with odds ratio estimated at 3.65 and 2.63, respectively. In a multivariate model, EAT remained independently associated with higher high-sensitivity C-reactive protein and fatty liver disease. Conclusions: These data suggested that echocardiography-based epicardial fat measurement can be clinically feasible and was related to several metabolic abnormalities and independently associated fatty liver disease. In addition, EAT amount may contribute to systemic inflammation beyond traditional cardiovascular risks and body fat composition. © 2012 by the American Society of Echocardiography. Source
Kuo C.-F.,Allergy and Immunology |
Kuo C.-F.,Chang Gung University |
Yu K.-H.,Allergy and Immunology |
Yu K.-H.,Chang Gung University |
And 7 more authors.
Rheumatology (United Kingdom) | Year: 2013
Objective: To investigate the association between gout and myocardial infarction (MI) in a representative cohort in Taiwan. Methods: Data were collected from the Taiwan National Health Insurance database. Adults >20 years of age without history of MI were included. Patients were considered to have gout if they received a diagnosis of gout requiring medical treatment. Multivariate Cox proportional hazards models were used to evaluate the risk of MI in gout patients. Results: Of the 704 503 patients included, 26 556 (3.8%) had gout. In total, 3718 (with gout, n = 463; without gout, n = 3255) patients had an MI, 299 (with gout, n = 35; without gout, n = 264) of whom died. The incidence of MI was 2.20 and 0.60 per 1000 patient-years in individuals with and without gout, respectively (log-rank test, P < 0.001). After adjustment for age, sex and history of diabetes mellitus, hypertension, coronary heart disease (CHD), stroke and end-stage renal disease, gout was associated with MIs [hazard ratio (HR), 1.23] and non-fatal MIs (HR, 1.26). In individuals without cardiovascular risk factors, gout was associated with MIs (HR 1.84; 95% CI 1.51, 2.24) and non-fatal MIs (HR 1.80; 95% CI 1.49, 3.95), after adjustment for age and sex. Moreover, in our study population, the HRs for MI decreased as age increased. Conclusion: Gout is an independent risk factor for MI, and the increased risk of MI is present even in young people and those without cardiovascular risk factors. © The Author 2012. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. Source
Liu C.-C.,National Taiwan University |
Liu C.-C.,Health Evaluation Center |
Hung C.-L.,National Taiwan University |
Shih S.-C.,Mackay Memorial Hospital |
And 2 more authors.
Health and Quality of Life Outcomes | Year: 2015
Background: Health intervention program (HIP) based on diet and lifestyle modifications had been shown to improve cardiovascular risks. The effects of such program on a variety of cardiometabolic outcome measures conducted in a strict analysis remained relatively unexplored. Materials and methods: A total of 2,660 participants (mean age: 43.3 ± 10 years, 63.6 % male) underwent annual health survey from our health evaluation department. We implemented health intervention program (HIP) in which diet and lifestyle modifications including smoking cessation and advised physical activities were introduced. We further studied the effects of HIP on several cardiometabolic outcome measures including Framingham, metabolic scores and renal function in terms of Egfr with a mean follow-up period of 38.5 months. Propensity score (PS) matching (HIP vs non-HIP group) was used to avoid effects of case selection bias. Results: Totally 1,004 (502 subjects for each group) left after PS matching protocol (both HIP and non-HIP group). The HIP group showed significant decline of waist circumference (-1.46 ± 0.61, p = 0.016), post-prandial glucose (-6.77 ± 2.06, p = 0.001), and total cholesterol level (-4.42 ± 2.15, p = 0.04), with borderline increase in eGFR (1.72 ± 0.94, p = 0.068) after an average of 1.91 ± 1.14 year follow up period. Exercise behavior significantly increased for those who received HIP when compared to the non-HIP group (44.6 vs 52.4 %, p = 0.014). PS matching and difference-in-difference (DID) analysis further confirmed the beneficial effects of ATP III reduction by HIP (-0.36 ± 0.06, p < 0.05). Conclusion: We demonstrated in our study that several cardiometabolic profiles can be substantially improved after health intervention introduction at the health evaluation center, supporting the beneficial evidence of such health intervention programs implementation based on primary prevention view points. © 2015 Liu et al. Source