Prevalence of metabolic syndrome Tsai TY et al. fat content, which serves as an indicator of obesity. In cases of obesity, adipose cells release free fatty acids and tumor necrosis factor-a (TNF-a), which blocks phosphatidylinosi- tide-3-kinase-dependent signal transduction pathways and reduces glucose uptake in the liver and skeletal muscles.6,27 To compensate, pancreatic b cells are induced to secrete excessive insulin, leading to hyperglycemia or type II diabetes. We discovered that ALT can better assess the risk of MS than AST, which is in line with both cross-sectional and cohort studies.28-29 This finding stems from the storage of ALT in hepatic cells; therefore, ALT is a more effective marker for detecting pathogenic hepatic fatty changes caused by obesity, as compared to AST.29 Two reasons may explain the positive relationship between ALT and the risk of MS. First, abnormally elevated ALT is often found in people under tremendous workplace pressure or extreme fatigue.30 High psychological pressure may activate the sympathetic system to raise arterial blood pressure and reduce renal blood flow.31 Consequently, the patient develops vasculitic reactions and elevated serum UA levels, increasing the risk of MS. Second, elevated ALT can also indicate abnormal liver function caused by fatty liver.28 Once a patient has developed fatty liver, fat accumulation has usually already occurred in the muscle and other organs, such as the pancreas. As these tissues release free fatty acids that inhibit the insulin-based regulation of the uptake and utilization of glucose, metabolic abnormalities subsequently emerge.27 This study found a positive correlation between WBC and the risk of MS, which was in line with previous literature reports.32-33 A higher WBC may be related to bacterial infection or vasculitis caused by hyperglycemia and dyslipidemia. In an inflammatory state, vascular endothelial cells secrete proinflammatory cytokines, such as interleukin- 6 or TNF-a, which can activate and attract massive numbers of white blood cells to the damaged region within the lumen of the vessel.33 Following infiltration into the tunica media, white blood cells absorb oxidized LDL-C and become foam cells, which may greatly increase the risk of thromboembo- lism. Additionally, Rho kinase secreted by white blood cells can serve as another potential pathogenic mechanism. Liu et al.32 have found that Rho kinase can block insulin signaling by stimulating the phosphorylation of insulin receptor substrate-1. This action prevents the translocation of glucose to the cell membrane by glucose transporter 4, thereby leading to insulin resistance. Our study revealed that workers with MS have a higher risk of elevated UA, which is in accordance with a previous report.34 The mechanism involved may be related to the ability of high levels of UA to inhibit the production of nitric oxide (NO) by endothelial cells. NO can serve as an inhibitor of thrombosis and inflammatory reactions, further preventing the growth and transfer of vascular smooth muscle cells.35 As for hemoglobin levels, we discovered that hemoglobin was of borderline significance. Because the specific biological mechanisms by which hemoglobin levels increase the risk of MS remain unclear, further study is needed to clarify the effect of hemoglobin levels on MS, especially among diverse participants. The results from this study should be interpreted with the following limitations in mind. First, subjects were drawn from a single company in southern Taiwan, and, therefore, the inferences drawn from the results are not completely 1534 CLINICS 2011;66(9):1531-1535 generalizable. More diverse samples collected by a nation- wide survey or random sampling should be considered in future research. Second, as a cross-sectional study, we cannot infer causality from our findings. A longitudinal study design is needed to investigate any causal relationships among the factors included in this study. Third, data on potential factors, such as smoking, alcohol, education, exercise habits, family history, and worksite pressure were not collected in this study; lack of information about these factors may have caused some inferential error. Future studies are needed to understand the impact of the abovementioned confounding variables on MS. Moreover, issues related to the medical costs induced by MS also warrant further evaluation. Despite these methodological concerns, to our knowledge, this was the first evidence-based study to estimate the prevalence of MS in Taiwanese high-tech industry workers. It also involved an analysis of corresponding health check-up data, which can be useful in assessing the risk factors for MS because the data were obtained from standardized laboratory tests. CONCLUSION This study explored the prevalence of MS and related factors among high-tech industry workers. We found that factors contributing to a high risk of MS included being male and older, as well as having a higher BMI, increased ALT, elevated UA, and higher WBC. If our study is replicated in other occupational settings, the results may have significant economic and public-health implications for other shift-work occupational groups, such as the military, medical service personnel, and police officers. We believe that our findings support the need to improve workplace health promotion in the high-tech industry. For example, appropriate on-site diet and exercise programs aimed at high-tech industry workers should be implemen- ted. In addition, occupational managers should actively offer in-service education concerning MS prevention to workers and monitor their physical and mental health, especially in high-risk cases. In summary, the identification of at-risk workers and disease management programs addressing MS-related factors are of great importance in employer-based interventions. ACKNOWLEDGMENT This study was supported by grants from the Buddhist Dalin Tzu Chi General Hospital. REFERENCES 1. World Health Organization. Cardiovascular Diseases. Available online: http://www.who.int/mediacentre/factsheets/fs317/en/index.html. Accessed 2010 Apr 25. 2. Leal J, Luengo-Ferna´ndez R, Gray A, Petersen S, Rayner M. Economic burden of cardiovascular diseases in the enlarged European Union. Eur Heart J. 2006;27:1610-9, doi: 10.1093/eurheartj/ehi733. 3. 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