Direct effect of glucocorticoids on glucose-activated adult rat β-cells increases their cell number and their functional mass for transplantation.

Compounds that increase β-cell number can serve as β-cell replacement therapies in diabetes. In vitro studies have identified several agents that can activate DNA synthesis in primary β-cells but only in small percentages of cells and without demonstration of increases in cell number. We used whole well multiparameter imaging to first screen a library of 1,280 compounds for their ability to recruit adult rat β-cells into DNA synthesis and then assessed influences of stimulatory agents on the number of living cells.

Glucose regulates rat beta cell number through age-dependent effects on beta cell survival and proliferation.

Background: Glucose effects on beta cell survival and DNA-synthesis suggest a role as regulator of beta cell mass but data on beta cell numbers are lacking. We examined outcome of these influences on the number of beta cells isolated at different growth stages in their population.

Methods: Beta cells from neonatal, young-adult and old rats were cultured serum-free for 15 days.

Beta cell count instead of beta cell mass to assess and localize growth in beta cell population following pancreatic duct ligation in mice.

Background: Pancreatic-tail duct ligation (PDL) in adult rodents has been reported to induce beta cell generation and increase beta cell mass but increases in beta cell number have not been demonstrated. This study examines whether PDL increases beta cell number and whether this is caused by neogenesis of small clusters and/or their growth to larger aggregates.

Methodology: Total beta cell number and its distribution over small (<50 µm), medium, large (>100 µm) clusters was determined in pancreatic tails of 10-week-old mice, 2 weeks after PDL or sham.