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Effects of Prolactin on Pancreatic Function in Mice

Research Project

Project/Area Number 63540596
Research Category

Grant-in-Aid for General Scientific Research (C)

Allocation TypeSingle-year Grants
Research Field 動物形態・分類学
Research InstitutionUniversity of Tokyo

Principal Investigator

MORI Takao  University of Tokyo, Faculty of Science, Zoological Institute, Associate Professor, 理学部, 助教授 (80011659)

Project Period (FY) 1988 – 1989
Project Status Completed (Fiscal Year 1989)
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)
Keywordsmouse / prolactin / hyperprolactinemia / pancreas / insulin / hyperinsulinemia / hyperglycemia / 高血糖
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.

Report

(3 results)
  • 1989 Annual Research Report   Final Research Report Summary
  • 1988 Annual Research Report
  • Research Products

    (11 results)

All Other

All Publications (11 results)

  • [Publications] T.Mori: "Pancreatic lesions in mice receiving ectopic pitnitary isograft" Int.J.Pancreatology,suppl 2. Vol.3. S221 (1988)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1989 Final Research Report Summary
  • [Publications] 守隆夫: "動物のホメオスタシス" 数理科学. 305巻. 58-63 (1988)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1989 Final Research Report Summary
  • [Publications] T.Mori: "prolactin gene family and its receptors の中の1章" Elesevier Suence Publishers B.V., 4 (1988)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1989 Final Research Report Summary
  • [Publications] T.Mori: "Cancer Growth and Progressionの中の1章" Kluwer Academic Press, 9 (1989)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1989 Final Research Report Summary
  • [Publications] T. Mori: "Pancreatic lesions in mice receiving ectopic pituitary isograft" Int. J. Pancreatology Vol.3; 221, 1988.

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1989 Final Research Report Summary
  • [Publications] T. Mori: "Effects of long-term treatment with prolactin on mammary gland, uterus and pancreas in SHN mice:Induction of multiple lesions." Prolactin Gene Family Elsevier Sci. Pub. pp.131-135, 1988.

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1989 Final Research Report Summary
  • [Publications] T. Mori and H. Nagasawa: "Multiple endocrine syndrome in SHN mice:Mammary tumors and uterine adenomyosis." Cancer Growth and Progression, Kluwer Academic Press, pp.121-130, 1989.

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1989 Final Research Report Summary
  • [Publications] T. Mori, H. Nagasawa and Y. Ohta: "Prolactin and uterine adenomyosis in mice." Prolactin and Lesions in Breast, Uterus and Prostae, CRC Press, Inc., pp.123-139, 1989.

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1989 Final Research Report Summary
  • [Publications] Mori,T.: "Cancer Growth and Progression中の1章" Kluwer Academic Press, 9 (1989)

    • Related Report
      1989 Annual Research Report
  • [Publications] T.Mori: Int.J.Pancreatology,Suppl.2. Vol.3. S221 (1988)

    • Related Report
      1988 Annual Research Report
  • [Publications] T.Mori: "Effects of long-term treatment with prolactin on mammary gland,uterus,and pancreas in SHN mice,In:Prolactin gene family and its receptors,K.Hoshino ed." Elsevier Science Publishers B.V., 131-135 (1988)

    • Related Report
      1988 Annual Research Report

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Published: 1988-04-01   Modified: 2016-04-21  

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