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From the Clinical Research Centers |
Division of Biostatistics (Y.H., T.R., D.C.R.), Washington University School of Medicine, St. Louis, Missouri 63110-1093; Physical Activity Sciences Laboratory (J.G., J.-P.D., L.P., C.B.), Laval University, Québec GIK 7P4, Canada; Lipid Research Center (J.-P.D.), Laval University, Quebéc GIV 492, Canada; Diabetes Research Unit (A.N.), Laval University, Quebéc GIV 492, Canada; School of Kinesiology and Leisure Studies (A.S.L.) University of Minnesota, Minneapolis, Minnesota 55455; Department of Kinesiology (J.S.S.), Indiana University, Bloomington, Indiana 46202; Department of Health and Kinesiology (J.H.W.), Texas A&M University, College Station, Texas 77843; and Departments of Genetics and Psychiatry (D.C.R.), Washington University School of Medicine, St. Louis, Missouri 63110
Address all correspondence and requests for reprints to: Dr. Yuling Hong, Division of Biostatistics, Campus Box 8067, Washington University School of Medicine, St. Louis, Missouri 63110. E-mail: yuling{at}wubios.wustl.edu
Abdominal visceral fat (AVF) is an obesity-related phenotype thought to be associated with insulin resistance, diabetes mellitus, and atherosclerosis. Significant genetic influences on both AVF and insulin levels have been reported. However, information is lacking as to whether common genetic influences on AVF and insulin levels exist.
AVF was assessed by computed tomography scan, and fasting insulin was measured by RIA in 512 members of 98 sedentary Caucasian families participating in the HERITAGE Family Study. Baseline data, collected before exercise training, were used in the present investigation. A bivariate familial correlation model was applied to evaluate whether there are familial influences that are common to insulin and AVF before and after adjustment for total fat mass (FM), and to assess the overall heritability of insulin and AVF. The maximal heritability for AVF, before and after adjustment for total FM, was 42% and 50%, respectively; and for insulin, it was 21%. Interestingly, 29% of the familial influences on insulin were also common to AVF, whereas 14% of the familial influences on AVF were shared by insulin. Furthermore, after AVF was adjusted for total FM, these common familial influences were increased to 48% and 20%.
Genes and/or familial nongenetic factors with pleiotropic effects seem to influence both AVF and plasma insulin levels to a certain degree. Genes involved in the regulation of lipid storage and mobilization in the abdominal fat depot are potential candidates for these genetic pleiotropic effects.
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