Assessing the role of visceral adipose tissue on pancreatic inflammation and function in zebrafish (2013)

Undergraduates: Ian Cassidy, Chris Harvey James Minchin

Faculty Advisor: John Rawls
Department: Biology

---

Obesity is a growing epidemic across the United States and around the world, increasing the risk for many diseases including heart disease, type II diabetes, and cancer. The probability of developing one of these diseases increases significantly as the body¿s levels of white adipose tissue (WAT) increase. Obesity is the increased storage of lipid in WAT, most particularly around internal organs such as the pancreas. Pancreatic WAT regulation has been implicated in the causes of pancreatitis, which is linked to incidences of type II diabetes. We conducted a zebrafish ENU mutagenesis screen to identify and evaluate adipose tissue mutants in order to gain a deeper understanding of the genetic regulation for adipocyte formation and function. Little is known today about the developmental and metabolic pathways that govern the storage of lipid in adipocytes and their subsequent mobilization in vivo. Our screen identified several lines of potentially mutant zebrafish: two of our most promising mutant lines had phenotypes consisting of ectopic fat in the liver and reduced pancreatic visceral WAT. By studying mutations in WAT regulation in the zebrafish model, we might identify potential novel gene targets that could reduce obesity and associated diseases.