| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1998: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1997: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Research Abstract |
Athough the existence of cholecystokinin-like immunoreactivity (CCK-LI) in the pancreas had been reported previously, it was never clearly demonstrated whether CCK is produced in pancreatic islets. The purpose of the study was to elucidate the source of the CCK-LI, the molecular properities of CCK, the expression of the CCK gene in islet cells, and the ontogeny of CCK during pancreatic development. The CCK-LI was found in the center of the islets, co-localized with insulin in B cells. The major molecular form of CCK in the islets was CCK-8. A350-nucleotide fragment of PCR-amplified CCK cDNA was detected in the islet as well as the duodenum by RT-PCR. In situ hybridization showed that CCK mRNA was located in a large portion of the islests, and this was consistent with the immunohistochemical findings. CCK-LI was first detected at E15, and was distributed in the periphery of the islets in the fetal and neonatal pancreas. The mirror sections for CCK and the absorption study revealed that CCK-LI in the fetal and neonatal pancreas was cross-reacting gastrin rather than CCK-8. From weaning (P21) through adulthood, on the other hand, CCK-LI was espressed diffusely in pancrealic islets, but there were no gastrin-positive cells after weaning. In situ hybridization showed that CCK mRNA was present in rat pancreatic islets in adults but not in early development. While CCK-positive cells were not detected in fetal and neonatal pancreatic islest, CCK was expressed in islets during and after weaning through adulthood, indicating that CCK in pancreatic islets might be developmentally regluated.
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