Dawn Coletta, PhD

Dr. Coletta is an Associate Professor in the College of Medicine at the University of Arizona.  She has a shared appointment between the Division of Endocrinology, Diabetes and Metabolism and the Department of Physiology.  In addition, Dr. Coletta is an Associate Professor in the Center for Disparities in Diabetes, Obesity, and Metabolism.  She joined the University of Arizona in August 2016.  Prior to joining the University of Arizona, Dr. Coletta was an Assistant Professor in the Center for Metabolic and Vascular Biology (CMVB) at Arizona State University (ASU), and prior to that an Assistant Professor in the Diabetes Division in the Department of Medicine at the University of Texas Health Science center at San Antonio (UTHSCSA). Dr. Coletta completed her Ph.D. degree at Aston University in Birmingham, England.  She completed her postdoctoral training at the Diabetes Division in the Department of Medicine at the University of Texas Health Science center at San Antonio (UTHSCSA).  

Dr. Coletta is an independent and highly productive scientist studying the molecular basis, genetics and epigenetics of insulin resistance. Dr. Coletta's work has been published in journals such as Diabetes, Diabetologia, Epigenetics, Obesity, Pediatric Obesity, Human Heredity, PLoS One, The Journal of Biological Chemistry and Clincal Epigenetics. Her work has been funded by the National Institutes of Health, American Diabetes Association and American Heart Association.  Dr. Coletta has been actively teaching for over 15 years.  She has been involved in curriculum development, directing and lecturing multiple courses, and mentoring students both in the classroom and laboratory.  Moreover, Dr. Coletta maintains a high level of service to the universities and to her field.

Research Interests

My primary research interests are to study the genetic and epigenetics of insulin resistance, which is a characteristic feature of a number of common metabolic diseases including type 2 diabetes mellitus, obesity and the insulin resistance syndrome. The prevalence of these complex metabolic diseases is rapidly and relentlessly increasing and to prevent the epidemic rise, it is necessary to define the genetic and epigenetic defects responsible for the insulin resistance that characterizes these common diseases. My laboratory combines state of the art techniques (global epigenetic mapping, oligonucleotide-based DNA chip microarray analysis, DNA resequencing, genomewide linkage analysis, single nucleotide polymorphism association studies, linkage disequilibrium mapping and mass spectrometry proteome analyses) and in vivo methods (euglycemic hyperinsulinemic clamp, muscle biopsies, exercise training, bariatric surgery, lipid infusion, drug intervention studies) to identify and characterize genes/loci that influence this complex phenotype. Susceptibility genes/loci identified from these analyses are characterized further using assays and molecular techniques that allow for functional analysis of each candidate gene. Identification of the genes that are critical to the development of insulin resistance will provide new targets for therapeutic interventions to reverse/ameliorate the insulin resistance and thereby lead to an improvement in these common metabolic diseases.