Roche C, Cordier-Bussat M, Ratineau C, Bernard C, Philippe J, Cuber J C
INSERM U45, Pavillon Hbis, Hôpital E. HERRIOT, 69437, Lyon Cedex 03, France.
Endocrine. 1996 Dec;5(3):331-4. doi: 10.1007/BF02739067.
The effects of the differentiation-inducing agent sodium butyrate on cholecystokinin (CCK) expression was investigated in the pancreatic islet tumor cell line RIN 1056E, which contains high levels of CCK-like immunoreactivity (CCK-LI). Exposure to butyrate for 24 h dose-dependently inhibited cell proliferation and increased the cell content in CCK-LI over the concentration range 0.1-8 mM. With 2 mM butyrate, cell proliferation was decreased by 50% and CCK-LI content was increased by 300%, whereas the level of steady-state CCK mRNA was reduced by 75%. Cycloheximide (10 μg/mL) abolished the sodium butyrate-induced increase in CCK-LI content. This article reports the novel finding that butyrate exerts opposite effects on CCK mRNA and immunoreactivity. The butyrate-induced increase in cellular CCK-LI content is entirely dependent on continuing protein synthesis.
