| Project/Area Number |
05670855
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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 |
内分泌・代謝学
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
TSUDA Kinsuke Kyoto Univ.Integrated Human studies, assistant professor, 総合人間学部, 助教授 (10180001)
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| Co-Investigator(Kenkyū-buntansha) |
SEINO Yutaka Kyoto Univ.Medicine.assistant professor, 医学部, 助教授 (40030986)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1993: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | insulin gene / transcription / CRE (CAMP response element) / CAMP / CRE(cyclic AMP response elenent) / cAMP / CRE(cyclic AMP rospone element) |
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| Research Abstract |
Diabetes mellitus is a disease of insulin deficiency. Insulin deficiency is caused by disturbances of insulin secretion and/or insulin action. The authors have published our data that suggest Japanese diabetic patients show hypoinsulinemia since early stage of diabetes mellitus. So to clarify the mechanism of insulin gene expression is very important. In this study we take the focus on the transcription of insulin gene because we have demonstrated that CREBP1 or c-Jun participate the insulin gene expression. We transfered the portion of DNA in the transcription region of human insulin gene into the fetal rat pancreatic beta cells and measured the transcription activities. We have the follwing results.
1) One mechanism of insulin gene induction by glucose is caused through cAMP.
2) The tanscription control of insulin gene by glucose have at least two mechanisms. One is related to CRE and one is not related to CRE.
3) HIT-T15 cell (hamster pancreatic beta cell line) have disturbance of cAMP signal transduction.
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