Subhadra Gunawardana, DVM, PhD

Associate Professor of Cell Biology and Physiology

Research Interests

Novel techniques for correcting type-1 diabetes without insulin, utilizing the beneficial effects of healthy adipose tissue: Subcutaneous transplantation of embryonic brown adipose tissue (BAT) has proven effective in reversing type 1 diabetes in mice, independent of insulin. Return to normoglycemia correlates with replenishment of healthy white adipose tissue, increased levels of beneficial adipokines and overall decrease of inflammation, while insulin remains consistently low. A physiological equilibrium of adipose tissue-derived factors appears to compensate for insulin. Ongoing work seeks to document the underlying mechanisms, and to customize this approach for human patients through establishing suitable alternatives for embryonic BAT.

Professional Education
  • BVSc: University of Peradeniya (Sri Lanka), 1991, Veterinary Medicine
  • MS: Iowa State University, 1995, Physiology
  • PhD: Cornell University, 2002, Pharmacology
  • Postdoc: Vanderbilt University, 2002-2007, Diabetes Research
Laboratory Affiliation

Piston Lab

South Building (MS: 8228-0003-04)

Fluorescence | Imaging | Quantitative Biology | Mathematical Models

Our lab focuses on understanding glucose-regulated hormone secretion from the islet of Langerhans, which is made up of glucagon secreting α-cells, insulin-secreting β-cells, and somatostatin-secreting δ-cells.  Recent work has uncovered glucagon’s critical role in glucose homeostasis and the pathology of diabetes.  Multiple signaling pathways arising from intrinsic glucose sensing, paracrine interactions and juxtacrine contacts within the islet all play a role in α-cell function.  Our lab develops quantitative fluorescence technology broadly applicable to cell, tissue, and whole-organism imaging experiments.  We apply these methods to assay living islet function quantitatively both ex vivo and in vivo, and these studies are proving critical to advancing our understanding of the regulation of glucagon secretion from α-cells.