Pancreatic a and b cells secrete glucagon and insulin respectively to maintain glucose homeostasis. In conditions that impair the signaling of these hormones, a and b cells compensate by increasing their number and augmenting their secretion. Defects in the compensatory responses lead to defects in glucose homeostasis. The molecular mechanisms underlying the compensatory responses remain incompletely understood. The Chen laboratory found that compensatory responses of pancreatic a cells and b cells is conserved in zebrafish, a vertebrate model amenable for live imaging as well as large-scale genetic and chemical screens. We combine genetic, pharmacological, and imaging techniques to identify genes essential for the compensatory responses and to define their roles in diabetes.


The following timeline graph is generated from all co-authored publications.

Most recent publication(s) are shown below:

  1. Conditional control of gene function by an invertible gene trap in zebrafish. Ni TT, Lu J, Zhu M, Maddison LA, Boyd KL, Huskey L, Ju B, Hesselson D, Zhong TP, Page-McCaw PS, Stainier DY, Chen W (2012) Proc Natl Acad Sci U S A 109(38): 15389-94
    › Primary publication · 22908272 (PubMed) · PMC3458342 (PubMed Central)
  2. Nutrient excess stimulates β-cell neogenesis in zebrafish. Maddison LA, Chen W (2012) Diabetes 61(10): 2517-24
    › Primary publication · 22721970 (PubMed) · PMC3447891 (PubMed Central)