Journal
HUMAN BIOLOGY
Volume 77, Issue 1, Pages 1-15Publisher
WAYNE STATE UNIV PRESS
DOI: 10.1353/hub.2005.0034
Keywords
hemostasis; diabetes; family study; heritability; Mexican Americans; San Antonio Family Heart Study; hemostasis-related traits; protein C; protein S; thrombin activatable fibrinolysis inhibitor (TAFI); prothrombin time; clotting factors; tissue factor pathway inhibitor (TFPI); Von Willebrand factor (VWF); activated partial thromboplastin time (APTT)
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Funding
- NCRR NIH HHS [M01-RR-01346] Funding Source: Medline
- NHLBI NIH HHS [HL70751, HL45522] Funding Source: Medline
- NIMH NIH HHS [MH59490] Funding Source: Medline
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Hypercoagulation often occurs in type 2 diabetes, suggesting pleiotropy of the genes that influence disease liability and hemostasis-related phenotypes. To better understand the relationship between hemostasis and diabetes, we first used maximum-likelihood methods to estimate the relative contribution of additive genetic, measured environmental, and shared household effects to the normal variance of 16 hemostasis-related traits in 813 individuals participating in the San Antonio Family Heart Study. We estimated moderate to high heritabilities (0.20-0.60) for each phenotype. Von Willebrand factor (VWF), thrombin activatable fibrinolysis inhibitor, activated protein C (APC) ratio, factor V and prothrombin time had heritabilities greater than 0.50. The correlation between type 2 diabetes status and the hemostasis-related traits was then partitioned into genetic and environmental components using bivariate variance-components methods. Significant (p <= 0.05) positive genetic correlations (0.37-0.51) occurred with factors 11 and VIII, VWF, total protein S (tPS), and tissue factor pathway inhibitor. Significant negative genetic correlations were estimated for activated partial thromboplastin time (-0.49) and APC ratio (-0.38). By contrast, significant environmental correlations occurred only with factor 11 (-0.40) and tPS (-0.31). Our results suggest that genes are important contributors to the normal variation in hemostasis-related traits and that genes influencing hemostasis-related traits pleiotropically influence diabetes risk.
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