• Search Research Projects
  • Search Researchers
  • How to Use
  1. Back to previous page

Study on the inhibitory control system of nonshivering thermogenesis by gene signal analysis.

Research Project

Project/Area Number 07670096
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Environmental physiology (including Physical medicine and Nutritional physiology)
Research InstitutionNayoro City College

Principal Investigator

YAHATA Takehiro  Nayoro City College, School of Nursing, Professor, 看護学科, 教授 (60041828)

Project Period (FY) 1995 – 1996
Project Status Completed (Fiscal Year 1996)
Budget Amount *help
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1996: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1995: ¥1,700,000 (Direct Cost: ¥1,700,000)
Keywordsbrown adipose tissue / glucagon / nonshivering thermogenesis / prolactin / prolactin receptor / mRNA / haloperidol / bromocriptine / 拘束ストレスラット / FOKラット / 酸素消費量 / ノルアドレナリン
Research Abstract

Brown adipose tissue (BAT) is the major site of nonshivering thermogenesis (NST) during cold acclimation. It is well established that the thermogenic activity of BAT is mainly regulated by sympathetic noradrenaline (NA) and pancreatic glucagon, but little is known about the factor concerning inhibitory control of BAT.Therefore, the present research was undertaken to evaluate the possibility of inhibitory role of prolactin (PRL) on BAT activity.
In male rats cold-exposure for 1 hr or 1 day decreased plasma PRL levels, but after cold-acclimation the plasma levels returned to the warm-acclimated control levels. Saline injection elevated the plasma PRL level and this elevation was blocked by noradrenaline (NA). In repeatedly-immobilized rats the elevation of plasma PRL level during immobilization stress was blocked. The resting plasma PRL level of genetically heat-tolerant FOK rats was lower as compared with those of other strains. In female animals haloperidol-treatment, causing hyper-prolactinemia, suppressed, while bromocriptine-treatment, causing hypo-prolactinemia, enhanced the in vitro responsiveness of BAT to glucagon, but not to NA.Dopamine mimicked the responses of BAT to bromocriptine. These results strongly suggest that PRL inhibits NST,especially by modifying the thermogenic action of glucagon in BAT.However, visible mRNA for PRL receptor was not detected in BAT.Further study on the subtypes of PRL receptor-mRNA is needed to clarify the role of PRL on BAT activity.

Report

(3 results)
  • 1996 Annual Research Report   Final Research Report Summary
  • 1995 Annual Research Report
  • Research Products

    (3 results)

All Other

All Publications (3 results)

  • [Publications] Clark M.Blatteis: "Thermoregulation Tenth International Symposium on the Pharmacology of Thermoregulation" New York Academy of Sciences, 875 (1997)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] T.Yahata, T.Nagashima, M.Moriya, A.Kuroshima, T.Kawada, F.Furuyama, and H.Nishino: Enhanced nonshivering thermogenic activity of the heat-tolerant FOK rat In "Thermoregulation Tenth International Symposium on the Pharmacology of Thermoregulation", C.M.Blatteis (ed). New York Academy of Science, 646-648 (1997)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Clark M.Blatteis: "Thermoregulation Tenth International Symposium on the Pharmacology of Thermoregulation" New York Academy of Sciences, 875 (1997)

    • Related Report
      1996 Annual Research Report

URL: 

Published: 1995-04-01   Modified: 2016-04-21  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi