J Korean Soc Endocrinol.
1999 Jun;14(2):255-264.
Effect of Isoproterenol on the Glucose-induced Hypothalamin Somatostatin Release
Abstract
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BACKGROUND: Acute hypoglycemia stimulates somatostatin
(SRIH) release from the hypothalamus, and which in turn
suppress growth hormone (GH) secretion from the anterior
pituitary gland. However, the exact mechanism of glucose
increases the hypothalamic SRIH secretion is not well known.
Beta-adrenergic pathway is known to stimulate the hypothalamus
SRIH release. We, therefore, hypothesized that the glucose-induced
SRIH release may be mediated by the stimulation of the central
beta-adrenergic system, and investigated to determine whether a
beta-adrermgic aganist, isoproterenol, contribute the suppressive
effect of glucose on the GHRH-induced GH secretian. METHODS: Ten
healthy young men, aged 23 to 26 years, were studied. Four
endocrinological tests were carried out. (Test 1) GHRH (Bachem,
CA, U.S.A.), 100pg bolus, was given intravenously at 0 minute.
(Test 2) Glucose 100 gm dissolved in water, was given orally at
-30 minute and GHRH was administered as Test 1. (Test 3) Isoproterenol
(Isuprel, Sanofi Winthrop, USA), 0.012 mg/kg, wasinfused continuously
between 0 minute and 120 minute, and GHRH was administered as Test 1.
(Test 4) Isoproterenol, 0.012 mg kg was infused continuously between 0
minute and 120 minute, and glucose and GHRH were administered as Test
2. RESULTS: Oral glucose ingestion significantly suppressed the GHRH-induced
GH secretion. The acute hyperglycemia significantly suppressed GHRH-induced
GH secretion. The pretreatments with isoproterenol significantly suppressed
the GHRH-induced GH levels. The pretreatment with glucose and isoproterenol
suppressed the GHRH-induced GH levels more compared to those induced by
glucose in Test 2. The GH levels in Test 4 did not significantly differ
from those in Test 3. CONCLUSION: The results of this study suggests that
the hypothalamic somatostatinergic activity induced by the oral glucose
administeration is not mediated by the beta-adrenergic pathway in normal
men. (J Kor Soc Endocrinool 14:255-264, 1999)