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Molly Bray, Ph.D.Molly S. Bray, Ph.D.

Associate Professor of Pediatrics
Baylor College of Medicine

PhD-- Human and Molecular Genetics
Graduate School of Biomedical Sciences
University of Texas-Houston

Genetics of Obesity, Leanness, and Exercise

Research Interests: 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.

Representative Publications:

Sailors MLH, Folsom AR, Ballantyne CM, Hoelscher DM, Jackson AS, Kao WHL, Pankow JS and Bray MS: (2007) Genetic variation and decreased risk for obesity in the Atherosclerosis Risk in Communities Study. Diab Obes & Metab.

Ferdinands JM, Mannino DM, Gwinn ML, Bray MS. (2007) ADRB2 Arg16Gly Polymorphism, Lung Function, and Mortality: Results from the Atherosclerosis Risk in Communities Study. PLoS ONE. 2007 2:e289

Grove ML, Morrison A, Folsom AR, Boerwinkle E, Hoelscher DM and Bray MS: (2007) Gene-environment interaction and the GNB3 gene in the Atherosclerosis Risk in Communities Study. Int J Obes (Lond). 31(6):919-26

Bray MS and Young ME: (2007) Circadian rhythms in the development of obesity: potential role for the circadian clock within the adipocyte. Obes Rev. 8: 169-181.

Young ME and Bray MS: (2007) Potential role for peripheral circadian clock dyssynchrony in the pathogenesis of cardiovascular dysfunction. Sleep Med.

Ioannidis JP, Gwinn M, Little J, Higgins JP, Bernstein JL, Boffetta P, Bondy M, Bray MS, et al. (2006) A road map for efficient and reliable human genome epidemiology. Nat Genet. 38:3-5.

Durgan DJ, Trexler NA, Egbejimi O, McElfresh TA, Suk HY, Petterson LE, Shaw CA, Hardin PE, Bray MS, Chandler MP et al.: (2006) The circadian clock within the cardiomyocyte is essential for responsiveness of the heart to fatty acids. J Biol Chem. 281: 24254-69.

Soliman PT, Wu D, Tortolero-Luna G, Schmeler KM, Slomovitz BM, Bray MS, Gershenson DM and Lu KH: (2006) Association between adiponectin, insulin resistance, and endometrial cancer. Cancer. 106: 2376-81.

Rankinen T, Bray MS, Hagberg JM, Perusse L, Roth SM, Wolfarth B and Bouchard C: (2006) The human gene map for performance and health-related fitness phenotypes: the 2005 update. Med Sci Sports Exerc. 38: 1863-88.

Ioannidis JP, Gwinn M, Little J, Higgins JP, Bernstein JL, Boffetta P, Bondy M, Bray MS, et al. (2006) A road map for efficient and reliable human genome epidemiology. Nat Genet. 38:3-5.

Wolfarth B, Bray MS, Hagberg JM, Perusse L, Rauramaa R, Rivera MA, Roth SM, Rankinen T and Bouchard C: (2005) The human gene map for performance and health-related fitness phenotypes: the 2004 update. Med Sci Sports Exerc. 37: 881-903.

Fornage M, Jacobs DR, Steffes MW, Gross MD, Bray MS and Schreiner PJ: (2005) Inverse effects of the PPAR(gamma)2 Pro12Ala polymorphism on measures of adiposity over 15 years in African Americans and whites. The CARDIA study. Metabolism. 54: 910-7.

Durgan DJ, Hotze MA, Tomlin TM, Egbejimi O, Graveleau C, Abel ED, Shaw CA, Bray MS, Hardin PE and Young ME: (2005) The intrinsic circadian clock within the cardiomyocyte. Am J Physiol Heart Circ Physiol. 289: H1530-41.

Heck AL, Barroso CS, Callie ME and Bray MS: (2004) Gene-nutrition interaction in human performance and exercise response. Nutrition. 20: 598-602.

Kao WHL, Coresh J, Shuldiner AR, Boerwinkle E, Bray MS, Brancati FL (2003) Pro12Ala of the peroxisome proliferator activated receptor-g2 gene is associated with lower serum insulin levels in non-obese African Americans: The Atherosclerosis Risk in Communities (ARIC) Study. Diabetes 52(6):1568-72.

Bray MS and Boerwinkle E: (2000) The role of beta(2)-adrenergic receptor variation in human hypertension. Curr Hypertens Rep. 2: 39-43.

Bray MS, Boerwinkle E and Hanis CL: (2000) Sequence variation within the neuropeptide Y gene and obesity in Mexican Americans. Obes Res. 8: 219-26.

Bray MS: (2000) Genomics, genes, and environmental interaction: the role of exercise. J Appl Physiol. 88: 788-92.