Molly Bray, PhD
Professor, Department of Epidemiology
School of Public Health
BS in Kinesiology, University of Houston, 1989
MEd in Exercise Physiology, University of Houston, 1991 - “Caltrac Validity for Estimating Energy Expenditure with Children,” Advisor: Dr. James Morrow, Jr.
PhD in Human and Molecular Genetics, University of Texas Graduate School of Biomedical Sciences,1998 - “Candidate Genes for Obesity in Mexican Americans from Starr County, Texas,” Advisor: Dr. Craig Hanis
University of Texas Institute of Molecular Medicine, 1998-1999, Advisor: Dr. Eric Boerwinkle
Molecular and genetic basis of obesity; genetic analysis of complex traits; gene-environment interaction; physical activity/exercise physiology; adipogenesis; genetics of response to obesity interventions
The work in my laboratory is focused on understanding the genetic basis of obesity using both statistical and experimental models. Obesity is one of the most profound public health problems today, with more than two thirds of the adults in the U.S. and more than 9 million children considered overweight or obese. Our lab is genotyping several large cohorts of obese and lean individuals for candidate polymorphisms within genes related to obesity and related comorbidities diseases (e.g. diabetes, NAFLD) using advanced high throughput genotyping techniques and the Illumina BeadStation. We are analyzing this genetic variation for association to obesity and related quantitative traits within the context of environmental factors.
Exercise is one of the first lines of both prevention and treatment for obesity, and our work also includes investigation of genetic factors that influence response to exercise training in a multi-racial population of students from the University of Houston. Participants in this study undergo 30 weeks of exercise training and are measured for a number of physiological parameters including body composition, blood pressure, heart rate, aerobic capacity, and blood lipids, glucose, insulin, and adipokines. The goal of this project is to identify genes that mediate the physiological changes that occur following exercise training.
Recent reports have suggested that altered sleep patterns associated with our "24-hour" lifestyle may contribute to the accumulation of body fat, although the mechanism for this association is not known. Work in our laboratory is designed to demonstrate the presence of a fully functional circadian clock within the adipocyte, and to identify the genes and metabolic functions that are regulated by this clock mechanism, with the ultimate goal of determining whether disease states precede (and therefore produce) or follow (and therefore are a consequence of) alterations in the clock mechanism. This work is being carried out through the use of microarray technology, quantitative real-time PCR in animal models, cultured tissues, and feeding studies. This research will provide important insight into the role of intrinsic clocks within adipose tissue in the development of obesity.
Relatively little is known regarding the metabolic consequences and molecular alterations that occur consequent to gastric bypass surgery in the pediatric population. We hypothesize that obesity produces molecular alterations in multiple tissues and that response to treatment both at the physiologic level as well as the level of gene expression may reveal a molecular fingerprint that defines 1) the genetic underpinnings of obesity; 2) the severity of related comorbidities; and 3) the probability of response to obesity treatment. This research is designed to evaluate genetic variation at both the level of DNA sequence and of gene expression in liver, adipose, and skeletal muscle prior to and following gastric bypass surgery in order to identify genetic factors leading to severe early onset obesity.
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