Abstract
Rat fetal pancreas development and maturation were investigated in vitro and in vivo, and the informations available on their controls do not agree. Our main objective was to reinvestigate fetal pancreas growth in vivo through treatments of the dams during their entire pregnancy. Pregnant rats were thus implanted subcutaneously with Alzet minipumps and received cerulein (0.25 μg kg<sup>–1</sup> h<sup>–1</sup>), gastrin-releasing peptide (GRP; 0.18 μg kg<sup>–1</sup> h<sup>–1</sup>), GRP antagonist (12 μg kg<sup>–1</sup> h<sup>–1</sup>), pentagastrin (2.38 μg kg<sup>–1</sup> h<sup>–1</sup>), L-365,260, a cholecystokinin B (CCK<sub>B</sub>) receptor antagonist (120 μg kg<sup>–1</sup> h<sup>–1</sup>), and hydrocortisone (417 or 833 μg kg<sup>–1</sup> h<sup>–1</sup>). After sacrifice at the end of pregnancy, the pancreata of the dams and those of their fetuses were excised for weight, protein, RNA, DNA, and digestive enzyme determinations. In the fetus, pancreas growth defined as hyperplasia was observed only in response to hydrocortisone, while aplasia occurred in response to cerulein. Gastrin and the GRP antagonist were the most effective hypertrophic agents, and the effect of the CCK<sub>B</sub> receptor antagonist was atrophic. In conclusion, hydrocortisone caused proliferation of the fetal rat pancreas, whereas gastrin induced its differentiation and maturation probably through CCK<sub>B</sub> receptor occupation.
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