This record provides bibliographic details and links to the original research. An editorial study breakdown is not available.
What the researchers found
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.
Why it matters
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.
How the study worked
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.
What this study cannot tell us
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.
Read the original research
Cholecystokinin expression in the β-cell leads to increased β-cell area in aged mice and protects from streptozotocin-induced diabetes and apoptosis.
American journal of physiology. Endocrinology and metabolism, 309(10), E819-28
Citation
Lavine, Jeremy A; Kibbe, Carly R; Baan, Mieke; Sirinvaravong, Sirinart; Umhoefer, Heidi M; Engler, Kimberly A; Meske, Louise M; Sacotte, Kaitlyn A; Erhardt, Daniel P; Davis, Dawn Belt. (2015). Cholecystokinin expression in the β-cell leads to increased β-cell area in aged mice and protects from streptozotocin-induced diabetes and apoptosis.. American journal of physiology. Endocrinology and metabolism, 309(10), E819-28. https://doi.org/10.1152/ajpendo.00159.2015