Before a person gets Type 1 diabetes, hormone-producing cell clusters within the pancreas become inflamed: Immune cells gang up on the beta cells, which normally pump out insulin, and start to destroy them. By the time the disease’s hallmark symptom — chronic hyperglycemia, or high blood sugar — manifests, 90 percent of the beta cells are gone.
Upfront is a quick look at the latest developments from Stanford Medicine.
A team of researchers from the School of Medicine has arrested that process in mice, using hymecromone, a compound already approved in Europe and Asia to treat gallbladder spasms.
Senior author Paul Bollyky, MD, PhD, assistant professor of infectious diseases, and his colleagues previously found that recently diagnosed Type 1 patients had an overabundance of hyaluronan molecules near their beta cells, whereas long-diagnosed patients did not. Administering hymecromone, which inhibits the body’s synthesis of hyaluronan, prevented the onset of hyperglycemia in mice prone to developing Type 1 diabetes; if it was withdrawn, they quickly became diabetic. Bollyky is planning to test the treatment in humans.
Research associate Nadine Nagy, PhD, is the lead author of the study, which was published in October in the Journal of Clinical Investigation.