Sarah A Aroner1, David E St-Jules1, Kenneth J Mukamal2, Ronit Katz3, Michael G Shlipak4, Michael H Criqui5, Bryan Kestenbaum3, David S Siscovick6, Ian H de Boer3, Nancy S Jenny7, Matthew J Budoff8, Joachim H Ix9, Majken K Jensen10. 1. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 2. Division of General Medicine and Primary Care, Beth Israel Deaconess Medical Center, Boston, MA, USA. 3. Division of Nephrology and Kidney Research Institute, Department of Medicine, University of Washington, USA. 4. Division of General Internal Medicine, University of California, San Francisco, USA. 5. Department of Family and Preventive Medicine, University of California, San Diego, USA. 6. The New York Academy of Medicine, New York, NY, USA. 7. Department of Pathology and Laboratory Medicine, University of Vermont College of Medicine, USA. 8. Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, USA. 9. Division of Nephrology-Hypertension, Department of Medicine, University of California, San Diego, CA, USA; Nephrology Section, Veterans Affairs San Diego Healthcare System, San Diego, CA, USA. 10. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA. Electronic address: mkjensen@hsph.harvard.edu.
Abstract
AIMS: Fetuin-A is a hepatic secretory protein that both promotes insulin resistance and inhibits arterial calcification. Previous studies have suggested that the association of fetuin-A with incident cardiovascular disease (CVD) might be modified by glycemic status. METHODS AND RESULTS: We conducted a case-cohort study of fetuin-A and incident non-fatal CVD nested in the Multi-Ethnic Study of Atherosclerosis with follow-up from 2000 to 2007. Fetuin-A concentrations were measured from baseline serum samples among 2505 randomly selected subcohort members and 142 incident cases. In weighted multivariable Cox regression models, no association was observed between fetuin-A and incident CVD in the total study population (HR per SD = 1.01; 95% CI: 0.84, 1.23). Although associations with CVD events were not statistically significant within categories of glycemic status, our results tended to support the interaction with glycemic status observed in other studies, with a positive trend restricted to participants with impaired fasting glucose or diabetes (HR per SD = 1.20; 95% CI: 0.89, 1.63) and an inverse trend among normoglycemic individuals (HR = 0.89; 95% CI: 0.69-1.13) (p-interaction = 0.04). In addition, we observed significant interaction between fasting glucose and fetuin-A when both were treated continuously in the subset of participants not using diabetes medication (p-interaction = 0.006). CONCLUSION: Our results suggest that fetuin-A is not associated with an overall risk of CVD, but support prior evidence indicating that the association might be modified by glycemic status.
AIMS: Fetuin-A is a hepatic secretory protein that both promotes insulin resistance and inhibits arterial calcification. Previous studies have suggested that the association of fetuin-A with incident cardiovascular disease (CVD) might be modified by glycemic status. METHODS AND RESULTS: We conducted a case-cohort study of fetuin-A and incident non-fatal CVD nested in the Multi-Ethnic Study of Atherosclerosis with follow-up from 2000 to 2007. Fetuin-A concentrations were measured from baseline serum samples among 2505 randomly selected subcohort members and 142 incident cases. In weighted multivariable Cox regression models, no association was observed between fetuin-A and incident CVD in the total study population (HR per SD = 1.01; 95% CI: 0.84, 1.23). Although associations with CVD events were not statistically significant within categories of glycemic status, our results tended to support the interaction with glycemic status observed in other studies, with a positive trend restricted to participants with impaired fasting glucose or diabetes (HR per SD = 1.20; 95% CI: 0.89, 1.63) and an inverse trend among normoglycemic individuals (HR = 0.89; 95% CI: 0.69-1.13) (p-interaction = 0.04). In addition, we observed significant interaction between fasting glucose and fetuin-A when both were treated continuously in the subset of participants not using diabetes medication (p-interaction = 0.006). CONCLUSION: Our results suggest that fetuin-A is not associated with an overall risk of CVD, but support prior evidence indicating that the association might be modified by glycemic status.
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