1Center for Neurobehavioral Genetics, University of California, Los Angeles, 2Department of Human Genetics, University of California, Los Angeles, 3Department of Pathology, Section on Comparative Medicine, Wake Forest School of Medicine
Thursday All day, Clinch Concourse
Obesity is a growing problem the world over, with a high cost to public health. This research investigates a baseline genetic predisposition to obesity during development in a genetically well-characterized model system: the vervet monkey (Chlorocebus aethiops sabaeus). We used basic measures taken thrice yearly on body size and composition such as BMI and waist circumference (WC) in a captive population of 657 monkeys measured from 2008 through 2012, to search for heritable patterns in obesity. We found that 43 (10% of adults) were chronically obese (obese during at least three successive measurements) with obesity defined as having an adult WC above 40.5 cm. Loess regressions and k-means clustering of longitudinal WC and BMI measures from 2000 to 2012 reveal stark differences in growth trajectories between chronically obese and non-obese colony members: whereas non-obese WC and BMI growth levels off just after attaining full adult size, obese colony members appear to maintain a pubertal growth slope up to a decade after puberty has passed. Analyses of estimated additive genetic heritability using SOLAR show that BMI, WC, and chronic obesity are all highly heritable (BMI: h2 = 0.65, p = 1.1 x10-09; WC: h2 = 0.61, p = 1.6 x 10-10; chronic obesity: h2 = 0.64, p < 0.01), at levels much higher than those seen in previous studies of NHP populations, with significant covariates represented by age and sex. This preliminary study suggests that more comprehensive examinations of growth may elucidate previously unknown patterns in the development of obesity.
This research benefitted from funding provided by the National Institutes of Health: RR019963/OD010965 (MJJ, JRK), RR016300 (NBF, AJJ, and CAS), 2T32NS048004-06A1 (CAS).