The purpose of this review is to explore the evidence accumulated thus far that suggests a genetic component to the observed variation in abdominal visceral fat (AVF) levels. The precise determination of AVF levels in humans is limited to methods such as computerized tomography and magnetic resonance imaging; thus, few studies have examined the role of genetic factors on this phenotype. Evidence from the Québec Family Study (QFS) and the HERITAGE Family Study indicates that between 50–55% of the variance in AVF levels, adjusted for total fatness, is attributable to genetic factors. Additionally, a major gene hypothesis for AVF was supported in the both the QFS and HERITAGE Family Study. However, after adjustment for total fat mass the support for a major gene was reduced, suggesting that a major gene which affects fat mass may also affect AVF either directly (pleiotropy), or indirectly. The search for candidate genes that may impact AVF levels is in its infancy, and few candidate genes have been identified. However, the glucocorticoid receptor (GRL), ß3 adrenergic receptor (ADRB3), and fatty acid binding protein 2 (FABP2) genes have been significantly associated with AVF or intra-abdominal fat levels in humans. In addition, three quantitative trait loci obtained from crosses of mice, the Do2, Mob4, and Qbw1 loci have been linked with mesenteric or abdominal fat and are thus considered positional candidate genes for AVF levels. The search for candidate genes or random genetic markers associated with AVF levels is a challenging prospect. However, given the significant heritability of this phenotype, the quest remains promising. Am. J. Hum. Biol. 11:225–235, 1999. © 1999 Wiley-Liss, Inc.
This chapter provides an overview of the basic study designs and research methods that can be used to investigate the genetic basis of human heterogeneity in the ability to benefit from a physically active lifestyle. It summarizes the key findings regarding the genetics of physical activity levels and responsiveness to regular exercise. It shows that genetic factors contribute to the individual differences in response to regular exercise.
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Physically fit individuals have a lower risk of cardiovascular disease and type 2 diabetes. However, it is unknown whether the associations between physical fitness and the metabolic syndrome are independent of total and abdominal adiposity. Physical fitness was defined as the physical work capacity on a cycle ergometer at heart rate of 150 bpm (PWC 150) in a sample of 158 men and 198 women 20-60 years of age. PWC 150 was adjusted for fat-free mass prior to the analyses. Percent body fat was estimated by hydrostatic weighing. Visceral and subcutaneous abdominal fat were measured by computed tomography. The prevalence of the metabolic syndrome was based on two definitions. The metabolic syndrome decreased with increasing fitness in men (approx. 6 times higher in less fit vs. most fit fertile, p < 0.05) and in women (approx. 4 times higher in less fit vs. most fit tertile, p < 0.05). Fitness was negatively associated with most individual components of the metabolic syndrome, except HDL-cholesterol for which the correlation was positive. However, in men and in women, the effects of physical fitness on the individual components of the metabolic syndrome were attenuated after considering total and abdominal adiposity. Key words: aerobic capacity, adiposity, abdominal fat, insulin resistance syndrome
