Regulation of neuropeptide Y expression by parathyroid hormone
| Project/Area Number |
18K19658
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Review Section |
Medium-sized Section 57:Oral science and related fields
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| Research Institution | Fukuoka Dental College |
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Principal Investigator |
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| Project Period (FY) |
2018-06-29 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2019: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2018: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
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| Keywords | parathyroid hormone / glucose transporter / osteoblasts / osteocytes / energy metabolism / Glucose transporter / Parathyroid Hormone / Neuropeptide Y / Osteocytes |
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| Outline of Final Research Achievements |
Parathyroid hormone (PTH) stimulates osteocytes to express neuropeptide Y (NPY). However, its physiological significance remains unknown. In this project, we investigated the role of NPY in energy metabolism of osteocytes and osteoblasts. We found that when osteocytes were exposed to PTH, genes related to the glucose transport were suppressed and that NPY is a center for this signaling pathway. Indeed, when NPY was deleted from osteocytes, glucose transporter genes such as Glut1 and Glut4 were activated. This suggests that the activation of NPY suppresses the transportation of glucose in osteocytes in response to PTH, resulting in slowing energy metabolism in osteocytes.
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| Academic Significance and Societal Importance of the Research Achievements |
副甲状腺ホルモンは生体カルシウム恒常性の維持を司る重要なホルモンである．副甲状腺機能亢進症でホルモンの分泌が持続的に過多になると骨からカルシウムが吸収され続け骨粗鬆症になる．本研究では，この副甲状腺ホルモンが骨で最も多い骨細胞の糖代謝を神経ペプチドYを介して制御していることを明らかにした．このことは，副甲状腺ホルモンが生体のエネルギー代謝の調節に関与していることを示しているもので，糖尿病の病理進行にも影響している可能性がある．今後，副甲状腺ホルモンが糖尿病患者の病状進行にあたえる影響を明らかにすることで，糖尿病治療に対する新たなアプローチを確立していく所存である．
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Report
(3 results)
Research Products
(23 results)
