| Project/Area Number |
63540596
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
動物形態・分類学
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| Research Institution | University of Tokyo |
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Principal Investigator |
MORI Takao University of Tokyo, Faculty of Science, Zoological Institute, Associate Professor, 理学部, 助教授 (80011659)
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| Project Period (FY) |
1988 – 1989
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| Project Status |
Completed (Fiscal Year 1989)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1989: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1988: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | mouse / prolactin / hyperprolactinemia / pancreas / insulin / hyperinsulinemia / hyperglycemia / 高血糖 |
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| Research Abstract |
Prolactin treatment directly stimulates insulin release from B-cells of rat pancreatic islets in vitro and in vivo, whereas insulin is shown to stimulate prolactin secretion from uterine decidual cells and pituitary tumor cells in vitro. These findings indicate an intimate relationship between prolactin and insulin secretion. Thus, it is worthwhile examining the long-term effects of prolactin on pancreas in an animal model.
Inbred strains of BALB/c and SHN mice were used in these experiments. Male and female mice of these strains were grafted with anterior pituitaries single each at the pancreata at 50 days of age and used at various intervals after the transplantation. Control mice of these strains were given a piece of submaxillary gland each at the same site. All grafts were obtained from the 50-day-old male mice of the respective strains.
Ectopic pituitary transplantation resulted in an elevation of plasma prolactin level, hyperprolactinemia, and an increase in the pancreatic weight, mainly due to hyperplastic proliferation of the pancreatic acinar glands. In addition, blood glucose levels in the mice with pituitary grafts were higher than in mice without pituitary grafts. On the other hand, serum insulin levels in mice with pituitary grafting were significantly higher than in mice without pituitary grafts. Pituitary grafting also induced an significant enlargement of the liver weight.
It is widely recognized that any conditions leading to hyperglycemia are highly related to pancreatic tumorigenesis. The present results imply that hyperprolactinemia associated with hyperglycemia is one of the causes of pancreatic tumorigenesis. In conclusion, the high circulating level of prolactin induced by the ectopic pituitary grafting plays an important role in the development of pancreatic hyperplasia.
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