The aim of the present study was to ascertain if reduced central serotoninergic activity might contribute to the well-known blunted growth hormone (GH) response to GH-releasing hormone (GHRH) in obese patients. Thus, we studied the effect of prolonged stimulation of the serotoninergic system by fenfluramine (FF; 60 mg twice daily for 7 days) on GHRH-induced GH release in nine obese and seven normal subjects. In controls, GHRH (100 μg intravenously [IV]) injection increased GH levels from 2.3 ± 1.8 (±SE) to 18.5 ± 2.8 mU/L, P < .002. FF administration enhanced both basal and GHRH-stimulated GH levels (peak, 38.4 ± 8.3 v 6.9 ± 2.6 mU/L, P < .002). This response was significantly higher (P < .02) than in pretreatment. In obese patients, GH responsiveness to GHRH was slight (peak, 7.1 ± 2.0 v 0.6 ± 0.18 mU/L, P < .01) and lower (P < .01) than in controls. FF administration did not affect this response. In controls, the enhanced FF-induced GH release after a maximal dose of GHRH indicates that serotoninergic activation influences GH secretion and that the mechanism involved is independent of endogenous GHRH. In obese patients, we found a blunted GH responsiveness to GHRH that was not affected by FF, thus supporting the hypothesis that the serotoninergic control on GH release is impaired.
Blunted growth hormone (GH) responsiveness to GH-releasing hormone (GHRH) in obese patients: influence of prolonged administration of the serotoninergic drug fenfluramine
BERNINI, GIAMPAOLO;
1991-01-01
Abstract
The aim of the present study was to ascertain if reduced central serotoninergic activity might contribute to the well-known blunted growth hormone (GH) response to GH-releasing hormone (GHRH) in obese patients. Thus, we studied the effect of prolonged stimulation of the serotoninergic system by fenfluramine (FF; 60 mg twice daily for 7 days) on GHRH-induced GH release in nine obese and seven normal subjects. In controls, GHRH (100 μg intravenously [IV]) injection increased GH levels from 2.3 ± 1.8 (±SE) to 18.5 ± 2.8 mU/L, P < .002. FF administration enhanced both basal and GHRH-stimulated GH levels (peak, 38.4 ± 8.3 v 6.9 ± 2.6 mU/L, P < .002). This response was significantly higher (P < .02) than in pretreatment. In obese patients, GH responsiveness to GHRH was slight (peak, 7.1 ± 2.0 v 0.6 ± 0.18 mU/L, P < .01) and lower (P < .01) than in controls. FF administration did not affect this response. In controls, the enhanced FF-induced GH release after a maximal dose of GHRH indicates that serotoninergic activation influences GH secretion and that the mechanism involved is independent of endogenous GHRH. In obese patients, we found a blunted GH responsiveness to GHRH that was not affected by FF, thus supporting the hypothesis that the serotoninergic control on GH release is impaired.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
