| Project/Area Number |
60480272
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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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 | KOBE UNIVERSITY |
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Principal Investigator |
CHIHARA Kazuo FACULTY OF MEDICINE, KOBE UNIVERSITY, 医学部, 助手 (00107955)
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| Project Period (FY) |
1985 – 1986
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| Project Status |
Completed (Fiscal Year 1986)
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| Budget Amount *help |
¥6,200,000 (Direct Cost: ¥6,200,000)
Fiscal Year 1986: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1985: ¥5,700,000 (Direct Cost: ¥5,700,000)
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| Keywords | Human growth hormone-releasing hormone / Radioimmunoassay / concentration in peripheral plasma / cerebrospinal fluid / Idiopathic growth hormone deficiency / Hypothalamic Lesion / 放射線療法 / 脳脊髄液 |
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| Research Abstract |
A sensitive RIA for human growth hormone-releasing hormone-(1-44)- <NH_2> (hGHRH) was developed which allow its measurement in extracts of human plasma and cerebrospinal fluid as well as various organ tissues obtained at autopsy. The highest concentration of GHRH-like immunoreactivity (GHRH-LI) was detected in extracts of median eminence and pituitarystalk whereas a small but significant amount of GHRH-LI was found in the pancreas, stomach, duodenum and jejunum. Oral ingestion of l-dopa and insulin-induced hypoglycemia caused a significant increase in both GHRH-LI and GH in peripheral circulation in normal subjects. The increase in plasma GHRH-LI slightly preceded or coincided with that in plasma GH. In patients with hypothalamic lesions, however, neither l-dopa ingestion nor insulin-induced hypoglycemia raised plasma GHRH-LI level. These findings suggest that the release by these stimuli ofhypothalamic GHRH into hypophysial portal circulation is reflected in changes in peripheral GHRH
… More
-LI levels. GHRH-LI was contained in cerebrospinal fluid(CSF) of normal subjects in a higher level than plasma, but undetectable in patients with hypothalamic lesion, suggesting that main source of GHRH-LI in CSF is the basal medial hypothalamus. In approximately 40% of idiopathic GH deficient dwarfism, plasma GHRH-LI rises after l-dopa ingestion were blunted and GHRH-LI level was extremely low , while the remaining 60% patients exhibited a significant GHRH-LI rise after l-dopa ingestion despite of moderately low GHRH-LI level in the CSF. GH deficiency on the former children is probably attributable to decreased hypothalamic GHRH secretion. The latter dwarfism might have the impaired somatotrophs in addition to the hypothalamic damage. Patients with active acromegaly had the GHRH-LI level in CSF comparable to that in normal subjects and exhibited plasma GHRH-LI increases after l-dopa ingestion as normal subjects did. Acromegalic patients previously treated with radiotherapy had significantly low GHRH-LI levels in the CSF and showed blunting plasma GHRH-LI response to l-dopa ingestion. Failure of suppressing hypothalamic GHRH release in active acromegaly may cause not only further stimulation of both synthesis and release of GH but also augmentation of tumor growth. Less
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