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SUJEAN CHOI, PH.D.

Professor

Department of Biomedical Sciences

Dr. Choi received her Ph.D. from the University of Rochester, Rochester, NY in 1995. Afterwards, she was a postdoctoral fellow at the University of California San Francisco. In 1999, she joined the faculty in the psychiatry department at the University of Pittsburgh Medical School and then joined the faculty at Marquette University in October of 2007.

Despite the global obesity epidemic, there are no broadly effective treatments for obesity.  My research program has demonstrated that a novel peptide, pituitary adenylate cyclase-activating polypeptide (PACAP), administered into the brain can reduce body weight by suppressing food intake and increasing metabolism. Interestingly, the effects to reduce body weight following PACAP treatment are identical to those following leptin administration. Leptin is a well-studied peptide known to produce similar effects of reducing food intake and increasing metabolism.  For example, the complete lack of leptin in animals or humans leads to an obesity that can be fully reversed by simple leptin replacement. 

 

Although most forms of human obesity result in excessive leptin levels, there is little understanding as to how leptin signaling is impaired in obese individuals, which would be a key step towards developing future therapeutics. Therefore, my lab integrates our PACAP research in the brain to explore whether leptin function is connected and/or dependent in any way with PACAP function. 

 

Lab personnel

  • Brian Maunze (graduate student)

 

​Projects:

 

  • We are currently exploring the mechanistic interactions between neuropeptides (a novel neuropeptide, PACAP) and a circulating peptide hormone (a canonical obesity signal, leptin) in the hypothalamus on the regulation of feeding behavior and metabolism in order to understand whether their interdependent relationship may cause a lean state to become an obese state. 

 

  • We have previously shown that PACAP selectively inhibits hunger-driven feeding through actions in the hypothalamus whereas, it suppresses reward-driven feeding through actions in an entirely different region of the brain known as the nucleus accumbens.  With this dichotomy in brain regions we can now begin to identify the causes of obesity or eating disorders with greater precision and to allow for the pursuit of more effective therapeutics that target a specific feeding system.