Molly Bray

At UT Austin, Dr. Molly Bray is the Chair of the Department of Nutritional Sciences, a Professor in the department, and is the Susan T. Jastrow Chair for Excellence in Nutritional Sciences. She also is a fellow of the Margaret McKean Love Chair in Nutrition, Cellular and Molecular Sciences and the Jean Andrews Centennial Faculty Fellowship in Human Nutrition. 

Prior to joining UT Austin, she served as the director of the Heflin Center for Genomic Sciences Genomics Core Laboratory at the University of Alabama at Birmingham and the Children’s Nutrition Research Center at the Baylor College of Medicine Genetics Core Laboratory.  She is a first-generation graduate, and her research is focused on the genetics of obesity and response to obesity treatments.

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 14 million children age 6-16 yrs currently considered overweight or obese.  The underlying causes of this astounding epidemic are likely many, and simplistic explanations based on over-consumption and/or poor diet or lack of physical activity are inadequate to account for this dramatic and literal “growth” in our world population.  My lab is currently using advanced high throughput omics technologies to identify the predictors of obesity and response to obesity treatments, including diet and exercise. We are analyzing genetic variation, gene expression, and whole genome DNA methylation for association to obesity and related quantitative traits within the context of environmental factors.

Circadian clocks are intrinsically maintained molecular mechanisms that condition the cell to changes in its environment and confer a selective advantage by providing a mechanism for anticipation of change.  Though diurnal variations in adipokines and adipose tissue metabolism have been observed, little is known regarding the molecular mechanisms that influence such variations.  Thus, work in my laboratory is also designed 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.  Based on studies in our lab in which the timing of macronutrient intake was manipulated in animals, a bolus of energy intake at the end of the waking period is associated with altered metabolism and obesity.