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Richard Benninger, PhD

Associate Professor - Bioengineering

Contact Information

Office: M20 - 4306D
Telephone: 303-724-6388

Curruculum Vitae: Download (pdf)​

Benninger Research Lab Website​​

Research Focus

Optical microscopy; Pancreatic islet biology and biophysics; Diabetes

My research interests are to develop and apply quantitative fluorescence microscopy approaches and predictive mathematical modeling to understand how the islet of Langerhans functions and how its dysfunction causes diabetes.

A predictive and quantitative model is a key component in the development of any systems biology approach; to link complex data as well as to generate new hypotheses by making quantitative predictions of future experiments. We develop advanced microscopy techniques and apply these to generate quantitative data about a biological system. These data can be used to test and refine current mathematical models of the biological system, and then generate new quantitative hypotheses that can be tested.

The biological system we are studying is the islet of Langerhans. Cellular destruction or defects in hormone secretion in the islet underlie the development of diabetes: a disease afflicting close to 400 million people world-wide. The islet is a multi-cellular micro organ and we are examining how communication between cells in the islet enhances the regulation of insulin and glucagon secretion to maintain glucose homeostasis. The overall goal is to be able to control cell-cell communication to improve the regulation of insulin and glucagon secretion to treat and cure diabetes, as well as to develop non-invasive diagnostics for diabetes.​​

  • Understanding emergent multi-cellular dynamics in the islet of Langerhans using confocal & two-photon microscopy, microfluidic devices, fluorescent protein biosensors and optogenetics. Computational models are developed and refined to describe these dynamics and put forward testable quantitative predictions regarding the coupled behavior of the islet.
  • Understand intra-islet regulation of insulin and glucagon secretion. Test how disruption to these mechanisms contributes to the pathogenesis of diabetes and whether modulating these mechanisms can blunt the progression of diabetes.
  • Develop and apply imaging and spectroscopy approaches for diagnostics in diabetes and other biomedical applications
  1. Phase transitions in the multi-cellular regulatory behavior of pancreatic islet excitability. Thomas H. Hraha, Matthew J. Westacott, Marina Pozzoli​, Aleena M. Notary, P. Mason McClatchey, Richard K.P. Benninger. PLoS Computational Biology (2014)  10 e1003819.​
  2. Fluorescence recovery after photobleaching reveals regulation and distribution of connexin36 gap junction coupling within mouse islets of Langerhans. Nikki L. Farnsworth, Alireza Hemmati, Marina Pozzoli​, Richard K.P. Benninger. Journal of Physiology (2014)  592 pp4431-46.​
  3. Decreasing Cx36 gap junction coupling compensates for overactive KATP channels to restore insulin secretion and prevent hyperglycemia in a mouse model of neonatal diabetes. Linda M. Nguyen, Marina Pozzoli, Thomas H. Hraha, Richard K.P. Benninger.  Diabetes (2014) 63(5) pp1685-97.
  4. Dimensionality and size scaling of coordinated Ca2+ dynamics in pancreatic β-cell clusters. Thomas H. Hraha, Abigail B. Bernard, Linda M Nguyen, Kristi S. Anseth, Richard K.P. Benninger.  Biophysical Journal (2014) 106 pp299-309.​
  5. Connexin-36 gap junctions regulate in-vivo first and second phase insulin secretion dynamics and glucose tolerance in the conscious mouse. W. Steven Head, Meredith L. Orseth, Craig S. Nunemaker, Leslie S. Satin, David W. Piston, Richard K.P. Benninger. Diabetes (2012)  6 pp1700-07

Vanderbilt University. Research Instructor. 2009-2011. Molecular Physiology and Biophysics.
Vanderbilt University. Post-Doctoral Research Fellow. 2006-2009. Molecular Physiology and Biophysics.
Imperial College London. PhD. 2002-2006. Physics (Optics and Biophysics).
Imperial College London. MSci. 1998-2002. Physics