Cholecystokinin expression in the β-cell leads to increased β-cell area in aged mice and protects from streptozotocin-induced diabetes and apoptosis.

Transgenic mice expressing cholecystokinin specifically in pancreatic β-cells showed increased β-cell area with age and were resistant to streptozotocin-induced diabetes due to reduced β-cell apoptosis. Additionally, CCK overexpression in cultured β-cells protected them from cytokine-induced apoptosis, indicating a protective autocrine/paracrine role of CCK in β-cell survival.

Researchers created a transgenic mouse model (MIP-CCK) that expresses CCK in pancreatic β-cells under lean conditions. They assessed β-cell area and apoptosis in aged mice and after streptozotocin treatment, a chemical that induces diabetes. They also tested CCK overexpression effects in cultured β-cells exposed to cytokines.

Understanding how CCK protects β-cells from apoptosis could lead to new diabetes treatments that preserve insulin-producing cells. Since CCK receptor agonists are being explored for obesity and diabetes, this study highlights their potential to directly safeguard β-cells.

The study was conducted in mice, so results may not fully translate to humans. The exact signaling mechanisms by which CCK protects β-cells were not fully elucidated. The evidence strength and study type were not specified.