Bernal-Mizrachi Receives New Grants for Studies of Type 1 and Type 2 Diabetes In Vivo
JDRF Funds Beta Cell Reprogramming Research, NIDDK Supports Examination of Glucose Intolerance
Dr. Ernesto Bernal-Mizrachi
ANN ARBOR, January 2011 — University of Michigan physician and faculty member Ernesto Bernal-Mizrachi, M.D., the Larry D. Soderquist Professor and Associate Professor of Internal Medicine in the Division of Metabolism, Endocrinology & Diabetes (MEND), has received two new research grants. One grant, from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) in the National Institutes of Health (NIH), will allow study of type 2 diabetes (usually associated with overweight adults). A second grant, from the Juvenile Diabetes Research Foundation (JDRF), will fund research into type 1 diabetes (also called juvenile diabetes).
From the NIDDK, Dr. Bernal secured over $1.3 million in funding for the project “Nutrient Signals and Programming of the Endocrine Pancreas.” The four-year project will study the processes by which certain conditions in the womb increase the potential for the fetus to develop glucose intolerance and type 2 diabetes during adult life. Although a primary developmental problem with beta cells has been described in the research literature, the overall in utero process for the increased susceptibility to diabetes is not yet well understood.
The goal of this research project is to describe the mechanisms responsible for regulating pancreas development and beta cell programming by nutrient signals, in an effort to develop strategies to prevent diabetes in growth-retarded fetuses — as well as to identify how drugs could potentially improve beta cell mass and function.
The project "In Vivo Reprogramming of Acinar to Beta Cells” was awarded $750,000 in funding from the Juvenile Diabetes Research Foundation (JDRF). The objective of this three-year research project is to explore how acinar cells in the pancreas can be converted to beta cells for those with type 1 diabetes, which is caused by destruction of beta cells. The role of acinar cells is to synthesize and secrete digestive enzymes, while beta cells secrete hormones. Previous research with mice has shown that neighboring cells, while having a different function but in the same organ, can be reprogrammed to function like their neighbor cells. “This approach is better in several ways,” states Dr. Bernal. “It will avoid the need for suppression of the immune system — because these are the subject’s own cells, not a donor’s. And it may provide an unlimited source of beta cells for type 1 diabetes patients.”
Dr. Bernal and his team will manipulate critical signaling pathways to trigger this acinar-to-beta-cell conversion in the pancreas of genetically-engineered mice. These experiments also will identify some of the downstream events responsible for this process. A desired outcome of this project is to eventually design drugs to induce acinar cell reprogramming, for the treatment and cure of type 1 diabetes.
Dr. Bernal-Mizrachi earned his M.D. degree from Universidad del Valle in Cali, Colombia, and received his internal medicine training at the University of Miami Jackson Memorial Hospital. Dr. Bernal-Mizrachi then accepted a fellowship in endocrinology at Washington University in St. Louis, MO, where he became an assistant professor of medicine. He joined the MEND Division at U-M in 2009.
For more information on Dr. Bernal's research, please see his lab website.