Benninger receives $3.5M in NIH research grants to study diabetes

Richard Benninger, Assistant Professor in the Department of Bioengineering, has been awarded two NIH Research Project (R01) grants from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). These two grants are to the amount of $1,749,375 and $1,749,375 in total costs, each over 5 years. Each research project grant focuses on studying the islets of Langerhans and their dysfunction in different forms of diabetes. Diabetes, a disease that afflicts close to 400M people world-wide, is characterized by a loss of glucose homeostasis which can lead to many diabetic complications including blindness, kidney disease, cardiovascular disease and limb amputations. Almost all cases of diabetes results from dysfunction to the insulin secreting beta cells in the islets of Langerhans, leading to insufficient secretion of the hormone insulin which regulates blood glucose homeostasis. Most treatments for diabetes therefore aim to prevent, restore or replace the disrupted secretion of insulin.

The first R01-funded project entitled “Emergent multi-cellular properties regulating pancreatic islet function” will apply quantitative fluorescence microscopy approaches, optogenetics and computational modelling to examine the cell signaling dynamics underlying insulin secretion from the islets of Langerhans. Specifically this project will focus on characterizing functional sub-populations of beta cells and determining how specific subpopulations of cells can exert disproportionate control over multiple functions of the islet through coupled dynamic processes; in healthy conditions and diabetic conditions caused by single gene mutations.

The second R01-funded project entitled “Multicellular interactions and dynamics of pancreatic islet function in diabetes” will examine dysfunction to the islets of Langerhans and regulation of insulin secretion during the progression of type2 diabetes. Specifically this project will focus on the important role of gap junction channels which mediate electrical communication between insulin-secreting beta cells. This includes characterizing the role of gap junction channel disruption in islet dysfunction during the progression of type2 diabetes, and determining ways gap junction coupling can be modulated to prevent the decline in beta cell mass and recover glucose-stimulated insulin secretion.

Together these projects will examine different ways that the function of the islets of Langerhans are disrupted in diabetes and discover strategies in which islet function can be restored; towards developing new treatments for different forms of diabetes.