Traci A. Czyzyk-Morgan, Ph.D.

Traci A. Czyzyk-Morgan, Ph.D., studies the physiology of obesity. There are currently very limited pharmacological treatment options for long-term weight loss management. Her laboratory utilizes multidisciplinary and integrative approaches to build better preclinical models to study the control of food intake and body weight.

Dr. Czyzyk aims to identify novel proteins and pathways that control energy and glucose homeostasis and that contribute to the development of metabolic syndrome, including fatty liver disease.

Dr. Czyzyk's laboratory uses a variety of in vivo physiology techniques, including indirect calorimetry and glucose clamp analysis. This work relies on both the availability of existing mouse models of obesity and diabetes and the generation of novel genetically engineered mouse strains within her laboratory.

Her laboratory also performs a variety of in vitro techniques to understand energy homeostasis at the cellular and molecular level, including culturing of hepatic cells and quantitative analysis of DNA, RNA and protein from ex vivo preparations.

Focus areas

• Determining what drives repeated binge-like eating behavior. Dr. Czyzyk's laboratory uses a mouse model of binge-like eating behavior to identify factors that precipitate and maintain binge behavior. Using both genetic and pharmacological approaches, she is exploring receptor systems (including opioid receptors) that might mediate binge eating disorder in humans. Further, her laboratory is incorporating behavioral and molecular models of drug addiction to better understand how "binge foods" (such as palatable high-fat and high-sugar foods) might rewire the brain in a way that is similar to the neuroadaptations seen with repeated use of abused substances, such as alcohol and cocaine.
• Determining how binge eating is contributing to the current obesity epidemic. Dr. Czyzyk's laboratory aims to determine how repeated exposure to binge-like eating behavior in mice can alter peripheral lipogenesis and energy expenditure in such a way that causes the animal to store more fat above and beyond what can be accounted for simply by increased caloric intake. Such metabolic adaptations would, over time, increase the incidence of obesity and type 2 diabetes.
• Determining how Mpzl3 can control energy and glucose homeostasis. While a postdoctoral fellow, Dr. Czyzyk showed that genetic ablation of Mpzl3 in mice reduces body weight and adiposity, increases energy expenditure, improves glycemic control, and abolishes the negative metabolic effects of exposure to a high-fat diet. Her laboratory is using both in vivo and in vitro approaches to determine the mechanisms by which Mpzl3 controls metabolic physiology. For example, her laboratory is using in vivo delivery of siRNAs in mice to knock down Mpzl3 expression to determine its function in specific tissues.

Significance to patient care

The overall goal of Dr. Czyzyk and her team is to better understand the physiology of obesity with the hopes of identifying novel pathways that could be targeted to cause weight loss in humans.

A majority of drugs are tested for efficacy based on their ability to reduce 24-hour food intake in preclinical models, but this is based on the assumption that there are normal circadian feeding patterns in people who are overweight.

Thus, identifying drugs that reduce food consumption in specific models of abnormal food intake might lead to a better success rate for developing weight-loss therapies.