Quabbe H J, Bunge S, Walz T, Bratzke B
Department of Internal Medicine, Klinikum Steglitz, Freie Universität, Berlin, West Germany.
J Clin Endocrinol Metab. 1990 Apr;70(4):908-15. doi: 10.1210/jcem-70-4-908.
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 micrograms/L at 60 min (P less than 0.001), and the mean plasma cortisol concentration from 320 +/- 55 to 700 +/- 133 nmol/L at 90 min (P less than 0.001). The mean plasma PRL concentration (basal value, 5 +/- 2.3 micrograms/L) did not change significantly. During glucose-induced hyperglycemia, the mean plasma GH concentration oscillated between 2.0-5.2 micrograms/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 micrograms/L at 270 min (P less than 0.001). During lipid-induced plasma FFA elevation, the mean plasma GH concentration decreased consistently from 6.5 +/- 1.0 micrograms/L to values between 1.3 +/- 0.2 and 2.6 +/- 0.6 micrograms/L from 60-360 min (P less than 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.
在11只自由活动的恒河猴和5只爪哇猴中，研究了血浆生长激素（GH）、催乳素（PRL）和皮质醇对血浆葡萄糖和游离脂肪酸（FFA）浓度抑制和升高的反应。通过慢性颈静脉导管采血并进行输注，导管经旋转接头延伸至相邻房间。在恒河猴中，胰岛素诱导的低血糖期间，血浆GH平均浓度在60分钟时从4.7±1.9微克/升升至17.4±2.5微克/升（P<0.001），血浆皮质醇平均浓度在90分钟时从320±55纳摩尔/升升至700±133纳摩尔/升（P<0.001）。血浆PRL平均浓度（基础值为5±2.3微克/升）无明显变化。葡萄糖诱导的高血糖期间，血浆GH平均浓度在60 - 360分钟内于2.0 - 5.2微克/升之间波动（无明显变化）。个别动物在高血糖期间出现大的GH分泌峰。烟酸诱导血浆FFA抑制期间，血浆GH平均浓度在270分钟时从3.7±0.6微克/升升至17.9±2.3微克/升（P<0.001）。脂质诱导血浆FFA升高期间，血浆GH平均浓度在60 - 360分钟内从6.5±1.0微克/升持续降至1.3±0.2至2.6±0.6微克/升之间（P<0.01）。血浆PRL和皮质醇浓度不受血浆FFA变化影响。与先前研究的一组恒河猴的自发血浆GH模式相比，低血糖和血浆FFA抑制期间血浆GH平均浓度升高。血浆FFA升高时强烈抑制，高血糖时轻度抑制。爪哇猴中观察到类似效应，不过未进行高血糖测试。我们得出以下结论。1）在恒河猴和爪哇猴中，与人类一样，GH分泌受血浆FFA抑制刺激，受血浆FFA升高抑制。在这两个物种中，急性低血糖刺激GH和皮质醇分泌。2）这些非人灵长类动物与人类的不同之处在于，高血糖在恒河猴中对GH分泌的抑制作用微弱（如果有抑制作用的话）（爪哇猴未进行高血糖测试），且在这两个物种中急性低血糖均不刺激PRL分泌。3）这两种灵长类动物均可作为人类GH分泌代谢调节的模型，尽管高血糖的抑制作用仍有待证实。
