Hormonal control of rat fetal pancreas development

Rat fetal pancreas development and maturation were investigated in vitro an d in vivo, and the informations available on their controls do not agree. O ur main objective was to reinvestigate fetal pancreas growth in vivo throug h treatments of the dams during their entire pregnancy. Pregnant rats were thus implanted subcutaneously with Alzet minipumps and received cerulein (0 .25 mu g kg(-1) h(-1)), gastrin-releasing peptide (GRP; 0.18 mu g kg(-1) h( -1)), GRP antagonist (12 mu g kg(-1) h(-1)), pentagastrin (2.38 mu g kg(-1) h(-1)), L-365,260, a cholecystokinin B (CCKB) receptor antagonist (120 mu g kg(-1) h(-1)), and hydrocortisone (417 or 833 mu g kg(-1) h(-1)). After s acrifice at the end of pregnancy, the pancreata of the dams and those of th eir fetuses were excised for weight, protein, RNA, DNA, and digestive enzym e determinations. In the fetus, pancreas growth defined as hyperplasia was observed only in response to hydrocortisone, while aplasia occurred in resp onse to cerulein. Gastrin and the GRP antagonist were the most effective hy pertrophic agents, and the effect of the CCKB receptor antagonist was atrop hic. In conclusion, hydrocortisone caused proliferation of the fetal rat pa ncreas, whereas gastrin induced its differentiation and maturation probably through CCKB receptor occupation.