Co-Chair:
Sushil G. Rane, NIDDK

Natcher Conference Center - Balcony A

Beta-cell mass regulation represents a critical issue for understanding diabetes, a disease characterized by a near-absolute (Type 1) or relative (Type 2) deficiency in the number of pancreatic beta cells. Replacing missing insulin-producing beta cells to treat diabetes is a major challenge for regenerative medicine. Beta-cell neogenesis from progenitor cells inside or outside islets and beta-cell replication represent potent mechanisms to expand beta-cell mass. However, it is critical to ensure that any surrogate or regenerated beta cells have perfectly regulated insulin production, which is essential for physiological glucose homeostasis. A better understanding of beta-cell biology and beta cell regeneration potential is needed to derive these specialized cells in sufficiently large numbers for therapy.

Program:

Islet Biology in Type 2 Diabetes
Josephine Egan, NIA

Role of the M3 Muscarinic Acetylcholine Receptor in Beta-Cell Function and Glucose Homeostasis
Jurgen Wess, NIDDK

Overlapping Techniques to Assess Human Pancreatic Beta Cell Regenerative Potential
David M. Harlan, NIDDK

Pancreas-derived Mesenchymal Stem Cells as Endocrine Progenitors
Marvin Gershengorn, NIDDK

Regulation of Beta-cell Biology by Cell Cycle Regulators
Sushil G. Rane, NIDDK