2016 Fiscal Year Final Research Report
Adrenocortical remodeling develops autonomous production of aldosterone
Project/Area Number |
26461387
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Endocrinology
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Research Institution | Keio University |
Principal Investigator |
MUKAI KUNIAKI 慶應義塾大学, 医学部(信濃町), 専任講師 (80229913)
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Keywords | アルドステロン / ステロイドホルモン / 副腎 |
Outline of Final Research Achievements |
Aldosterone is secreted from adrenal cortex in mammals and has an essential role for homeostasis of body fluid volume. Formation of excessive aldosterone-producing lesions such as adrenal adenomas causes primary aldosteronism in humans. This study focused on pathogenesis of primary aldosteronism and examined excessive aldosterone-producing lesions from patients by using histochemical methods and gene mutation analyses. The results suggested that an aldosterone-producing cell-cluster, which we previously discovered in normal human adrenal cortex, could develop to a transitional lesion further growing to an adenoma. Somatic mutations of a group of ion channel/pump genes were likely to play key roles for development from an aldosterone-producing cell-cluster to an adenoma through such a transitional lesion.
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Free Research Field |
生化学
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