Tarantini B, Ciuoli C, Checchi S, Montanaro A, Bonato V, Theodoropoulou A, Pasqui L, Pacini F
Section of Endocrinology and Metabolism, Department of Internal Medicine, Endocrinology and Metabolism and Biochemistry, University of Siena, Via Bracci, 53100 Siena, Italy.
J Endocrinol Invest. 2009 Apr;32(4):335-7. doi: 10.1007/BF03345723.
Ghrelin is an orexigenic hormone produced in the stomach and in other organs, exerting a wide range of metabolic functions, including stimulation of GH secretion. Ghrelin secretion is decreased by iv or oral glucose load as well as during euglycemic-hyperinsulinemic clamp and hypoglycemia. We evaluated the circulating ghrelin levels in GH-deficient (GHD) and in GH-sufficient (GHS) patients during GHRH plus arginine test.
The study group comprised 35 patients, including 20 with pituitary tumors, 12 with empty sella, 2 with short stature, and 1 with post-traumatic isolated GH deficiency. According to the results of GHRH plus arginine test, 14 patients were defined as GHD and 21 as GHS. Patients with central hypothyroidism, hypocorticism, and hypogonadism had been on replacement therapy for at least 3 months at the moment of the study. Blood samples were collected every 20 min up to 60 min after GHRH and arginine administration.
By definition, GH response to GHRH plus arginine was higher in GHS than GHD group (p<0.0001). Basal serum ghrelin levels were not different in the two groups and did not correlate with body mass index, GH, IGFI and insulin concentrations. After GHRH plus arginine, serum ghrelin decreased significantly in both groups, with percent decreases ranging 13.3-66.6% in GHD patients (p=0.001) and 7.2-42.2% in GHS patients (p=0.004), with no significant difference in the two groups (p=0.12).
Our results show that ghrelin secretion is not modulated by acute GH increase observed in GHS subjects during GHRH plus arginine infusion. The similar decrease of serum ghrelin after GHRH plus arginine stimulation in both GHS and GHD subjects demonstrated that there is no negative feedback of GH on ghrelin secretion.
胃饥饿素是一种在胃及其他器官产生的促食欲激素,具有广泛的代谢功能,包括刺激生长激素(GH)分泌。静脉注射或口服葡萄糖负荷以及在正常血糖 - 高胰岛素钳夹试验和低血糖期间,胃饥饿素分泌会减少。我们评估了生长激素释放激素(GHRH)加精氨酸试验期间生长激素缺乏(GHD)和生长激素充足(GHS)患者的循环胃饥饿素水平。
研究组包括35例患者,其中20例患有垂体肿瘤,12例为空蝶鞍,2例身材矮小,1例为创伤后孤立性生长激素缺乏。根据GHRH加精氨酸试验结果,14例患者被定义为GHD,21例为GHS。中枢性甲状腺功能减退、肾上腺皮质功能减退和性腺功能减退患者在研究时已接受至少3个月的替代治疗。在给予GHRH和精氨酸后,每20分钟采集一次血样,直至60分钟。
根据定义,GHS组对GHRH加精氨酸的生长激素反应高于GHD组(p<0.0001)。两组的基础血清胃饥饿素水平无差异,且与体重指数、生长激素、胰岛素样生长因子I(IGFI)和胰岛素浓度均无相关性。给予GHRH加精氨酸后,两组血清胃饥饿素均显著下降,GHD患者下降百分比为13.3 - 66.6%(p = 0.001),GHS患者为7.2 - 42.2%(p = 0.004),两组间无显著差异(p = 0.12)。
我们的结果表明,在GHRH加精氨酸输注期间,GHS受试者中观察到的急性生长激素增加并未调节胃饥饿素分泌。GHS和GHD受试者在GHRH加精氨酸刺激后血清胃饥饿素的类似下降表明,生长激素对胃饥饿素分泌不存在负反馈。