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Czyzyk Lab

Traci A. Czyzyk, Ph.D.
Assistant Professor, Physiology, Mayo Clinic in Arizona

There are currently very limited pharmacological treatment options for long-term weight loss management. The ultimate goal of the Czyzyk laboratory 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. To do this, the laboratory integrates a variety of in vivo techniques including indirect calorimetry (for the analysis of whole-body energy expenditure), hyperinsulinemic clamp analysis (to assess insulin sensitivity and hepatic glucose production) and behavioral phenotyping (to study the relationships between food intake, mood and whole-body energy metabolism). This work relies on both the availability of existing mouse models of obesity and the generation of genetically engineered mouse strains. The 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 cell cultures and ex vivo preparations.

One of the main interests in the Czyzyk lab is the development of novel preclinical rodent models of obesity that can be used to identify efficacious weight loss drugs. The most common model used is the diet induced obese rodent, where mice or rats are fed a high-fat and sugar diet for several weeks to induce obesity. However, this model assumes that 1) obesity has a single etiology and 2) that normal circadian feeding patterns are intact in obesity. The identification of drugs that reduce food consumption in specific models of abnormal food intake might lead to a better success rate for developing weight-loss therapies. The Czyzyk lab uses a novel, stress-free mouse model of binge-like eating behavior to identify factors that precipitate and maintain binge behavior, and to determine how binge-eating is contributing to the current obesity epidemic. For example, does repeated exposure to binge-like eating behavior 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 by simply increased caloric intake? Such metabolic adaptations would, overtime, increase the incidence of obesity and Type 2 diabetes. The lab also aims to identify new receptor systems (such as opioid receptors) that may be effective in treating binge eating disorder in humans using both genetic and pharmacological approaches.

The Czyzyk laboratory is also interested in using genetic mouse models to identify novel proteins and pathways that control energy and glucose homeostasis. During her postdoctoral fellowship, Dr. Czyzyk determined that the putative cell-adhesion molecule MPZL3 is a critical regulator of hepatic lipogenesis and whole-body energy expenditure in mice. 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. The Czyzyk laboratory is currently using viral overexpression and siRNA knockdown techniques in vivo and in vitro to determine how Mpzl3 functions to control energy balance.

Lab Members

Postdoctoral Fellows
Petr Telensky, Ph.D.

Technical Staff:
Natalie Barker, B.S.
James Krantz, B.S.
Alysia Polito, B.S.

Undergraduate Assistants
Tiffany Tang