Mark O. Huising

Mark O. Huising, PhD, Professor, Neurobiology, Physiology and Behavior Physiology and Membrane Biology, University of California, Davis

Research Description: One of the signals studied by the Huising lab is called Corticotropin Releasing Factor (CRF), a stress peptide initially identified as the main hypothalamic factor that triggers the stress response by acting on the pituitary gland. Interestingly, insulin-producing beta cells in the pancreas can directly respond to CRF, leading to increased insulin release, enhanced beta cell growth, and reduced cell death under inflammatory conditions—an encouraging set of benefits from a single molecule. Urocortin3 (Ucn3), a peptide related to CRF, is highly expressed by mature beta cells. The lab discovered that Ucn3 is co-released with insulin and triggers somatostatin release from nearby delta cells, which then inhibits insulin secretion. This creates a negative feedback loop, reducing insulin secretion once glucose levels are adequately lowered. Additionally, Ucn3 distinguishes mature, functional beta cells from their immature precursors, a property that is particularly useful for tracking the development of mature, glucose-responsive beta cells from embryonic or induced pluripotent stem cells. CRF and Ucn3 are just two examples of signaling molecules that act directly on the pancreas, adding complexity to the network of signals regulating beta cell mass and the pancreas’s insulin and glucagon production. My team aims to uncover the impact of these local pancreatic CRF family signaling pathways on glucose metabolism in both healthy and diabetic individuals.