On April 18, 2016, the Naomi Berrie Diabetes Center held its annual Diabetes Research Symposium, an evening that showcases the depth and scope of the science conducted at the Berrie Center. “The Berrie Center is designed to conduct basic research in the physical context of clinical care,” said Rudy Leibel, MD, the Christopher J. Murphy Professor of Diabetes and the Berrie Center Co-Director. “The work of this Symposium spans the spectrum of what is relevant to diabetes at the research bench and in the clinic.”
This year’s panelists included Domenico Accili, MD, the Russell Berrie Foundation Professor of Diabetes, Chief of the Endocrinology Division, and Director of the Columbia University Diabetes and Endocrinology Research Center. He spoke of his discovery several years ago (since replicated by several other labs) that gut cells could be converted to insulin-producing cells, and talked about just how close we are now to clinical trials of a drug that will do the same in people.
Dieter Egli, PhD, Maimonides Assistant Professor of Diabetes Research, a stem cell biologist and expert on the creation of patient-specific stem cells, talked about stem cell-derived beta cells - what many scientists believe to be the key to curing diabetes. “We have made a lot of progress in making patient-specific beta cells that can respond to glucose and secrete insulin,” Dr. Egli said. “We have made human stem-cell derived beta cells that can reverse diabetes in a mouse.”
Panelist Nichol Danzl, PhD, M Phil, explained how she works with a humanized mouse model to study the immune system of people with type 1 diabetes (T1D). “We transplant cellular components of the human immune system into a mouse and we are able to see how a person’s immune system will respond in our model,” she said. Dr. Egli added, “Our priority is to cure T1D.” According to Dr. Egli, a cure for T1D means that “your body takes care of itself and regulates blood sugar without the attention of the patient. “ We are trying to teach the immune system, first in the humanized mouse, and eventually in a patient with T1D, to tolerate highly functional transplanted beta cells.”
Anthony Ferrante, MD, PhD, Dorothy & Daniel Silberberg Associate Professor of Medicine, explained how his studies of adipose (fat) tissue are designed to better understand the important contributions of this tissue to normal and abnormal metabolism related to body weight and diabetes. He is, for example, studying how the types of immune cells that relate to inflammation, and infiltrate adipose tissue, affect its metabolic function.
Rebecca Haeusler, PhD, Assistant Professor of Pathology and Cell Biology, also participated in the panel. She is investigating why people with diabetes have a higher risk for cardiovascular disease. Her work has revealed previously unknown roles for bile acids in this susceptibility.
The evening belonged to the audience, their questions, and the panelists’ responses. “This research symposium was certainly more electric than some of its predecessors, with the passions that are often politely suppressed given opportunity for expression,” Dr. Leibel said of this year’s Q&A, “it is very important to let these views and concerns be aired.”
The first question came from Mary Elizabeth Bunzel, who along with Paul Healy and Alka Singh sponsored the Diabetes Research Panel. She asked, “Why should we care about the intersections of type 1 diabetes and type 2 diabetes in research and clinical care?” Dr. Egli explained that “they are both diseases of the beta cell. “In both instances the beta cells become stressed and die. We are interested in learning why, because if you can reverse that process you could cure or prevent both type 1 diabetes and type 2 diabetes.”
The question provoked vigorous, in some instances contentious, responses from the audience, particularly around the differences in the clinical severity of these two types of diabetes. The differences in clinical severity were contested by others in the audience who had type 2 diabetes. The panel members were sympathetic and emphasized again the convergent relevance of basic beta cell biology to all types of diabetes, and the similarity of many of the medical complications of all types of diabetes.
The audience was interested in learning how Berrie Center researchers share their research—a question that was answered by Dr. Ferrante. “Under the leadership of Berrie Center Co-Directors Rudy Leibel and Robin Goland, collaboration is fostered locally by a tradition of sharing and free exchange of ideas and resources, and at an international level through weekly conferences and an annual symposium.”
According to the panelists, the number one threat to the finding a cure is the decline in research funding from the NIH, which must be compensated for by private donations for progress to continue. Said Dr. Accili, “We’ve lost a quarter of our purchasing power in the last 10 years.” Added Dr. Leibel, “Novel work is not funded by conventional resources because they are more conservative by their very nature. This is a very expensive enterprise.”
In closing the Symposium, John Eastman, a Chair of the Diabetes Advisory Board (along with Jodie, Jay and Katama Eastman), made a pledge of $100,000 toward diabetes research and clinical programs at the Berrie Center that he hoped would be matched with an additional $400,000 of donations. This $500,000 would inaugurate his plan to lead a 2 year, $5 million campaign in behalf of faculty development and research and clinical programs of the Center.
If you are interested in making a donation to the Naomi Berrie Diabetes Center, please contact Jamie Gutter, director of development at firstname.lastname@example.org.