Associate Professor, Departments of Pediatrics and Molecular and Human Genetics

B.S., University of Houston, 1989
M. Ed., University of Houston, 1991
Ph.D., University of Texas-Graduate School of Biomedical Sciences, 1998
Postdoc, University of Texas-Institute of Molecular Medicine, 1998-1999

RESEARCH INTERESTS:

The work in our 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.

SELECTED PUBLICATIONS:

1. Grove ML, Morrison A, Folsom AR, Boerwinkle E, Hoelscher DM, Bray MS (2007). Gene-environment interaction and the GNB3 gene in the Atherosclerosis Risk in Communities Study. Int. J. Obes. (Lond) 31: 919-926.

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

3. Sailors MLH, Folsom AR, Ballantyne CM, Hoelscher DM, Jackson AS, Kao WHL, Pankow JS, Bray MS. Genetic Variation and Decreased Risk for Obesity in the ARIC Study. Diab. Obes. Metab. 9: 548-57.

4. Rankinen T, Bray MS, Hagberg JM, Perusse L, Roth SM, Wolfarth B, Bouchard C (2006). The human gene map for performance and health-related fitness phenotypes: the 2005 update. Med. Sci. Sports Exerc. 38: 1863-1888.

5. Durgan DJ, Trexler NA, Egbejimi O, McElfresh TA, Suk HU, Petterson LE, Shaw CA, Hardin PE, Bray MS, Chandler MP, Chow CW & Young ME (2006). The circadian clock within the cardiomyocyte is essential for responsiveness of the heart to fatty acids. J. Biol. Chem. 281: 24254-24269.

6. Soliman PT, Wu D, Tortolero-Luna G, Schmeler KM, Slomovitz BM, Bray MS, Gershenson DM, Lu KH (2006). Association between adiponectin, insulin resistance, and endometrial cancer. Cancer 106: 2376-2381.

7. 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.

8. Zeng D, Lin DY, Avery CL, North KE, Bray MS (2006). Efficient semiparametric estimation of haplotype-disease associations in case-cohort and nested case-control studies. Biostatistics 7: 486-502.

9. Hsu CC, Bray MS, Kao WH, Pankow JS, Boerwinkle E, Coresh J (2006). Genetic Variation of the Renin-Angiotensin System and Chronic Kidney Disease Progression in Black Individuals in the Atherosclerosis Risk in Communities Study. J. Am. Soc. Nephrol. 17: 504-512.

For more publications, see listing on Pub Med.

CONTACT INFORMATION:

Molly Bray, Ph.D.
Department of Pediatrics
Children's Nutrition Research Center
Baylor College of Medicine
1100 Bates, Suite 8070
Houston, Texas 77030, U.S.A.

Phone: 713-798-9311
Fax: 713-798-7187
E-mail:

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