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Effect of Oral Glucose Administration on Plasma Growth Hormone-Releasing Hormone (GHRH)-Like Immunoreactivity Levels in Normal Subjects and Patients with Idiopathic GH Deficiency: Evidence that GHRH Is Released Not Only from the Hypothalamus but Also from Extrahypothalamic Tissue^*

Third Division, Department of Medicine, Kobe University School of Medicine Kusunoki-Cho, Chuoh-Ku, Kobe 650, Japan

Address all correspondence and requests for reprints to: Dr. Yoichi Kashio, Third Division, Department of Medicine, Kobe University School of Medicine, 7-chome, Kusunoki-cho, Chuoh-Ku, Kobe 650, Japan.

Using a specific and sensitive RIA for GH-releasing hormone (GHRH), we examined the effect of oral administration of 75 g glucose on peripheral plasma GHRH-like immunoreactivity (GHRH-LI) in normal subjects (n = 12) and patients with idiopathic GH deficiency (IGHD) (n = 6). The normal subjects had two peaks of plasma GHRH-LI after oral glucose administration. The initial peak GHRH-LI levels occurred 30–150 min after glucose ingestion and corresponded to an increase in blood glucose. The increment in plasma GHRH-LI levels 30 min after glucose ingestion [7.4 ± 2.4 (±SEM) pg/ml] was significantly higher (P < 0.05) than that during a control study. Second peaks in plasma GHRH-LI occurred 3.5–6 h after glucose ingestion, and the mean increment 5 h after glucose ingestion was 9.4 ± 2.4 pg/ml. This second rise of plasma GHRH-LI coincided with a significant increase in plasma GH after reactive hypoglycemia.

This second GHRH-LI peak and the rise of plasma GH after hypoglycemia were absent in patients with IGHD, whereas the first peak of plasma GHRH-LI appeared shortly after glucose ingestion in these patients as well as in normal subjects. In addition, hypoglycemia produced by iv injection of regular insulin (0.1 U/kg) was not accompanied by increases in plasma GHRH-LI and GH levels in patients with IGHD, whereas insulin-induced hypoglycemia resulted in significant elevations of both plasma GHRH-LI and GH levels in normal subjects.

These findings suggest that 1) peripheral plasma GHRH-LI is derived from the hypothalamus as well as from an extrahy-pothalamic source(s); 2) extrahypothalamic GHRH is released shortly after glucose ingestion; and 3) secretion of GHRH from the hypothalamus is stimulated by hypoglycemia.

^* This work was supported in part by research grants from the Japanese Ministry of Health and Welfare; the Japanese Ministry of Education, Science, and Culture; and the Growth Science Foundation for 1984 and 1985.

Received February 21, 1986.

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