The Islet Biology/Insulin Secretion track at the 77th Scientific Sessions kicks off on Friday, June 9, with a mini-symposium titled Human Islet Research Network—NIH-Funded Interactive Research Network (12:45 p.m.–1:45 p.m.).
“There are things we can do in rodents that we can’t do in humans, but rodent models do not always recapitulate human biology,” said Lori Sussel, PhD, the member of the Scientific Sessions Meeting Planning Committee planning sessions in the area of islet biology/insulin secretion. “There are a variety of different causes of diabetes in type 1 and type 2, but it’s ultimately the islets that become dysfunctional. Understanding islet dysfunction in humans requires working through the details of human islet biology.”
Research into islet biology and insulin secretion is moving relentlessly into humans, added Dr. Sussel, Professor of Pediatrics and Director of Research at the Barbara Davis Center for Childhood Diabetes at the University of Colorado Anschutz Medical Campus. The growing availability of human tissues is allowing researchers to evaluate the human pancreas in physiological and pathophysiological conditions. And although there are many similarities to what was known from rodent studies, there’s a growing recognition that animal models do not fully recapitulate human biology.
“We need to keep working with islets from rodents and other species, but it’s time to take what we have learned and apply it to islets, pancreas sections, and other human tissues,” said Adolfo Garcia-Ocaña, PhD, Professor of Medicine at the Icahn School of Medicine at Mount Sinai. “This human-centric focus is producing important new information in islet biology, from development to signaling, insulin secretion, proliferation, gene regulation, and the impact of drugs that we are already using to treat diabetes.”
During another Friday session, Chemical Modulation of Beta-Cell Function (2:00 p.m.–4:00 p.m.), four speakers will explore drug discovery and drug-mediated changes in beta cells, from differentiation to proliferation and function.
“The focus of this session is to look at different aspects of how we can make more beta cells, more functional human beta cells,” Dr. Garcia-Ocaña said.
The track continues Saturday, June 10, with the Joint ADA/EASD Symposium – Current Diabetes Therapies Affecting the Islet (8:00 a.m.–10:00 a.m.). Antidiabetic drugs such as SGLT2 inhibitors, antiglucagon agents, and GLP-1 analogs can reduce glucose levels, but their effects on islets are less clear.
“These therapies are being widely used around the world, but there can be unexpected side effects on the pancreatic islets,” Dr. Sussel explained. “Some patients have had adverse responses and we’re using rodent models to understand how these drug therapies can affect the physiology of the pancreas.”
Another Saturday session, Novel Islet Signaling Pathways (4:00 p.m.–6:00 p.m.), will push the boundaries about what is known of islet signaling. Presenters will discuss new methods for protecting functional beta cells and inducing beta cell expansion.
“There are new approaches to protect beta cells from glucotoxicity and cytokine-mediated death, as well as new data on fatty acid signaling and what it means for both insulin secretion and beta cell proliferation,” Dr. Garcia-Ocaña said. “This symposium will provide exciting information on what signals to follow to protect and expand human beta cells and increase islet function.”
Other endocrine cell types also contribute to the organ system. A session on Monday, June 12, titled The Neglected Delta Cell (8:00 a.m.–10:00 a.m.), will showcase studies describing the importance of the somatostatin-producing delta cell in islet function and diabetes.
According to Dr. Sussel, one of the most important sessions in the track is a Monday afternoon symposium titled Pancreas Development Revisited from a Human Perspective (4:30 p.m.–6:30 p.m.). The session’s four expert presenters will discuss the transition from mouse models to human pancreatic development.
“A lot of past studies have been in mice, rats, monkeys, and other species,” Dr. Sussel said. “We are finally getting significant information from human tissues showing both the similarities and differences between animal and human architecture during fetal development. Not surprisingly, it turns out that pancreas development is not the same in mice and humans. Now that we have a better understanding of human islet development, we are able to more accurately model human islet development from human pluripotent stem cells and use this system to model human diseases such as monogenic diabetes.”