Ultradian growth hormone rhythm in the rat: effects of feeding, hyperglycemia, and insulin-induced hypoglycemia.
Ultradian growth hormone rhythm in the rat: effects of feeding, hyperglycemia, and insulin-induced hypoglycemia.
复制标题
大鼠的超生长激素节律：喂养、高血糖和胰岛素诱导的低血糖的影响。
作者：
G. Tannenbaum;J. B. Martin;E. Colle
通过采集携带慢性心内静脉插管的自由活动雄性大鼠的连续血液样本，确定血浆生长激素、免疫活性胰岛素(IRI)和血糖的时间模式。每15min采血一次，连续采血6h，用放射免疫法测定血浆GH和IRI。每只未受干扰的动物都有典型的生长激素分泌超常节律(峰值大于200 ng/ml，谷值小于1 ng/ml，平均周期为3.40±0.08h)。基础血浆IRI和血糖水平波动最小。空腹大鼠血浆GH与胰岛素抵抗指数、生长激素与血糖、胰岛素抵抗指数与血糖水平均无显著相关性。摄食动物的生长激素分泌节律模式(平均周期：3.12±0.16h；峰值>200 ng/ml；谷值<1 ng/ml)与非摄食动物的相似(平均周期：3.34±0.15 h；峰值>200 ng/ml；谷值<1 ng/ml)，尽管血浆IRI水平波动很大，进食的食物数量和大小差异很大。膳食摄入量和GH分泌突发量之间没有一致的关系。高血糖对生长激素节律的平均周期(3.25±0.08h)无明显影响，但半数高血糖大鼠的脉搏波幅明显降低。胰岛素诱导的低血糖导致生长激素脉冲幅度显著降低；然而，这种反应的模式并不一致。尽管生长激素反应的差异很大，但所有动物的血糖水平恢复的幅度和时间过程都是相似的。这些结果表明，大鼠生长激素的分泌主要受内源性超常节律的调节，这种节律不依赖于血糖或IRI水平的变化，并继续独立于摄食行为发挥作用。生长激素不太可能是该物种葡萄糖动态平衡的重要生理调节因子。
Temporal patterns of plasma GH, immunoreactive insulin (IRI), and glucose were defined by obtaining serial blood samples from freely-moving male rats bearing chronic intracardiac venous cannulae. Blood was withdrawn every 15 min for periods of 6 h. Plasma GH and IRI were determined by radioimmunoassay. The typical ultradian rhythm of GH secretion was evident in each undisturbed animal (peaks greater than 200 ng/ml; troughs less than 1 ng/ml; mean period: 3.40 +/-0.08 h). Basal plasma IRI and glucose levels fluctuated minimally. There was no significant correlation between plasma GH and IRI, GH and glucose, or IRI and glucose levels in unfed rats. The rhythmic GH secretory patterns of feeding animals (mean period: 3.12 +/-0.16 h; peaks greater than 200 ng/ml; troughs less than 1 ng/ml) were similar to those of non-feeding animals (mean period: 3.34 +/-0.15 h; peaks greater than 200 ng/ml; troughs less than 1 ng/ml) despite large fluctuations in plasma IRI levels and a wide variation in the number and size of the meals taken. No consistent relation was observed between the ingestion of meals and the bursts of GH secretion. The mean period of the GH rhythm was not significantly altered by hyperglycemia (mean period; 3.25 +/- 0.08 h), although the amplitude of the pulses of half of the hyperglycemic rats was markedly depressed. Insulin-induced hypoglycemia caused a significant depression in the amplitude of the GH pulses; however, the pattern of this response was not consistent. Despite wide variability in the GH response, the magnitude and time course of recovery of the plasma glucose levels was similar in all animals. These results suggest that GH secretion in the rat is regulated primarily by an endogenous ultradian rhythm which is not dependent on changes in plasma glucose or IRI levels, and continues to function independently of feeding behavior. It is unlikely that GH is an important physiologic regulator of glucose homeostasis in this species.