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Plasma Glucose and Free Fatty Acids Modulate the Secretion of Growth Hormone, but not Prolactin, in the Rhesus and Java Monkey^*

Section of Endocrinology, Department of Internal Medicine, Klinikum Steglitz, Freie Universität, Berlin West Germany

Address all correspondence and requests for reprints to: H.-J. Quabbe, M.D., Klinikum Steglitz, Hindenburgdamm 30, D 1000 Berlin 45, West Germany.

In 11 freely moving rhesus and 5 Java monkeys the plasma GH, PRL, and cortisol responses to suppression and elevation of plasma glucose and FFA concentrations were studied. Blood was sampled and infusions given via chronic jugular catheters, extended via a swivel into the adjacent room. In the rhesus monkeys, the mean plasma GH concentration rose during insulin-induced hypoglycemia from 4.7 ± 1.9 to 17.4 ± 2.5 µg/L at 60 min (P = 0.001), and the mean plasma cortisol concentration from 320 ± 55 to 700 ± 133 nmol/L at 90 min (P = 0.001). The mean plasma PRL concentration (basal value, 5 ± 2.3 µg/L) did not change significantly. During glucose-induced hyperglycemia, the mean plasma GH concentration oscillated between 2.0–5.2 Mg/L from 60–360 min (no significant change). Large GH secretory episodes occurred during hyperglycemia in individual animals. During nicotinic acid-induced plasma FFA suppression, the mean plasma GH concentration increased from 3.7 ± 0.6 to 17.9 ± 2.3 µg/L at 270 min (P = 0.001). During lipid-induced plasma FFA elevation, the mean plasma GH concentration decreased consistently from 6.5 ± 1.0 µg/L to values between 1.3 ± 0.2 and 2.6 ± 0.6 µg/L from 60–360 min (P = 0.01). Plasma PRL and cortisol concentrations were not affected by plasma FFA changes. Compared with the spontaneous plasma GH pattern in a previously studied group of rhesus monkeys, the mean plasma GH concentration was increased during hypoglycemia and plasma FFA suppression. It was strongly suppressed during plasma FFA elevation and slightly suppressed during hyperglycemia. Similar effects were observed in the Java monkeys, although hyperglycemia tests were not performed.

We conclude the following. 1) In rhesus and Java monkeys, as in man, GH secretion is stimulated by plasma FFA suppression and is inhibited by plasma FFA elevation. In both species, acute hypoglycemia stimulates the secretion of GH and cortisol. 2) These nonhuman primates differ from man in that hyperglycemia only weakly inhibits GH secretion in the rhesus monkey, if at all (Java monkeys had no hyperglycemia tests), and in neither species does acute hypoglycemia stimulate the secretion of PRL. 3) Both primate species can serve as models for the metabolic modulation of GH secretion in man, although a suppressive effect of hyperglycemia remains to be proven.

^* This work was supported by Deutsche Forschungsgemeinschaft. Preliminary results of this study were presented at the Seventh International Congress of Endocrinology, Quebec, Canada, July 1–7,1984.

Received March 13, 1989.

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