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Genetic and environmental influences on body fat distribution, fasting insulin levels and CVD: are the influences shared?

Published online by Cambridge University Press:  21 February 2012

Tracy L Nelson
Affiliation:
Department of Biobehavioral Health and Center for Developmental and Health Genetics, The Pennsylvania State University, PA, USA. tnelson@cahs.colostate.edu
George P Vogler
Affiliation:
Department of Biobehavioral Health and Center for Developmental and Health Genetics, The Pennsylvania State University, PA, USA.
Nancy L Pedersen
Affiliation:
Department of Biobehavioral Health and Center for Developmental and Health Genetics, The Pennsylvania State University, PA, USA; Division of Genetic Epidemiology, Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden; Department of Psychology, University of Southern California, Los Angeles, CA.
Yuling Hong
Affiliation:
Division of Genetic Epidemiology, Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden; Division of Biostatistics, Washington University, School of Medicine, St Louis, MO.
Toni P Miles
Affiliation:
Department of Family Practice, Division of Geriatrics, University of Texas Health Sciences Center-San Antonio, TX, USA.
Corresponding

Abstract

Central body fat distribution has been shown to be related to hyperinsulinemia, insulin resistance, hypertriglyceridemia, and atherosclerosis to a greater degree than general obesity. There are known to be both genetic and environmental effects on all components of this clustering. Whether these genetic effects are due to one set of genes in common to the components or whether genetic influences on insulin resistance and/or general/abdominal fatness ‘turn on’ other genes that affect other components of the syndrome is not clear. We analyzed data from the Swedish Adoption/Twin Study of Aging (60% female; monozygotic = 116, dizygotic = 202; average age 65 years) to determine whether there were genetic and/or environmental factors shared among general body fat distribution, abdominal body fat distribution, fasting insulin levels and cardiovascular disease. We found additive genetic effects in males to be significantly different from those in females with genetic effects accounting for variance in waist–hip ratio (males = 28%; females = 49%), body mass index (males = 58%; females = 73%), fasting insulin levels (FI) (males = 27%; females = 49%), and cardiovascular disease (CVD) (males = 18%; females = 37%). There were also shared genetic and environmental effects among all the variables except CVD, but a majority of the genetic variance for these measures was trait specific. Twin Research (2000) 3, 43–50.

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Copyright © Cambridge University Press 2000
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