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The present study was performed using an animal model suitable for examining human GH secretion (clinically healthy and conscious adult male rhesus monkey). Insulin hypoglycemia and other tests of GH stimulation or suppression elicit reactions similar to those in man. It can thus be assumed with a high degree of probability that the results obtained in the model are applicable to man.Electrostimulatory tests in the basal hypothalamus (6 electrodes) and amygdaloid nucleus (7 electrodes) of five healthy and conscious adult rhesus monkeys are in accordance with results from anaesthetized rats: Electrostimulation in the basal hypothalamus induces GH suppression followed by a poststimulatory increase. In the amygdaloid nucleus, it generates a heterogeneous pattern of GH secretion. Both he anterior and the basal amygdaloid nucleus contain areas with a stimulatory or suppressive influence on GH secretion. Though a stimulatory effect is achieved by the sole application of either insulin hypoglycemia or electrostimulation in the basal amygdaloid nucleus, their combination in one animal unexpectedly leds to suppression of the insulin-hypoglycemia-induced increase in plasma GH. Furthermore, a first attempt was made to modulate a central-nervous stimulation by metabolite infusions. Most of the combination glucose-infusion experiments yielded in part very marked glucose decreases before, during and after electrostimulation (thus increasing GH secretion). Hence no definite statement can be made about the modulatory effect of glucose. Basically, however, no significant modulatory influence appears to be exerted on the electrostimulatory plasma GH increase.During electrostimulation in the lateral hypothalamic area of one animal, a reproducible increase of the electrostimulatory plasma GH increment was achieved by glucose infusion. To elucidate this phenomenon, more extensive investigations should be done on the way the "glucose sensor cells" are working. Intravenous infusions of 8-hydroxybutyrate or a mixture of lipids and heparin (to achieve an FFA increase in blood) lead to marked suppression of both stimulatory and poststimulatory plasma GH increments. The elevation of FFA leads to a more pronounced modulation of the electrostimulatory plasma GH increase than the infusion of B-hydroxybutyrate. This study demonstrates the suitability of an animal model for more extensive studies that may contribute towards fully elucidating the regulation of human GH secretion.