Previous in vivo studies have suggested a long-term regulatory role for insulin in the exocrine pancreas. To directly study the long-term effects of insulin on the pancreas in vitro, we have used cultured AR42J cells, a rat cell line that is derived from a transplantable tumor of the acinar pancreas. Hormone-binding experiments with 125I-labeled hormones indicated that AR42J cells have insulin receptors, relatively fewer receptors for insulin-like growth factor II (IGF-II), and no detectable receptors for insulin-like growth factor I (IGF-I). Insulin at concentrations as low as 1 nM stimulated the growth of these cells, as measured by an increase in DNA and protein content, and in cell number. At 100 nM, where insulin had a maximal effect, the growth of AR42J cells was stimulated by 46.1 ± 10.9% (mean ± SEM, N = 11).Insulin increased the amylase activity of AR42J cells over the same concentration range that it stimulated growth; at 100 nM, insulin increased amylase by 91.0 ± 15.4% (mean ± SEM, N = 23). Immunoprecipitation of [35S]methionine-labeled proteins revealed that insulin induced a selective increase of amylase synthesis over general protein synthesis. These studies indicate, therefore, that insulin stimulates both growth and amylase synthesis of AR42J cells.
Insulin, via Its Own Receptor, Regulates Growth and Amylase Synthesis in Pancreatic Acinar AR42J Cells
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Joachim Mössner, Craig D Logsdon, John A Williams, Ira D Goldfine; Insulin, via Its Own Receptor, Regulates Growth and Amylase Synthesis in Pancreatic Acinar AR42J Cells. Diabetes 1 September 1985; 34 (9): 891–897. https://doi.org/10.2337/diab.34.9.891
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