Invitti C, Pecori Giraldi F, Tagliaferri A, Scacchi M, Dubini A, Cavagnini F
2nd Chair of Endocrinology, University of Milan, Centro Auxologico Italiano, Italy.
Clin Endocrinol (Oxf). 1993 Aug;39(2):213-6. doi: 10.1111/j.1365-2265.1993.tb01776.x.
Galanin is believed to play a role in the control of prolactin (PRL) secretion in the rat. Such a role is uncertain in humans where the neuropeptide is expressed by the corticotrophs. However, in clinical conditions of enhanced ACTH secretion, increased PRL levels are often observed. Therefore, we evaluated the effect of galanin infusion on serum PRL levels in patients with Cushing's disease and in control subjects. For comparison, the PRL responses to TRH and metoclopramide were also investigated in the same patients.
Four tests were performed: (a) 40-minute infusion of 0.3 micrograms/kg/min of galanin; (b) infusion of normal saline only; (c) metoclopramide test (10 mg as i.v. bolus); (d) TRH test (200 mg as i.v. bolus).
Twenty-four normal subjects and nine patients suffering from active Cushing's disease were investigated.
Serum concentrations of PRL were measured by radioimmunoassay on blood samples collected before and for 90 minutes after drug or saline administration.
Serum baseline PRL levels were superimposable in normal subjects and in patients with Cushing's disease. In normal subjects, infusion of galanin induced a distinct PRL increase compared to saline (mean +/- SEM incremental areas 6514 +/- 2572 vs 540 +/- 571 mU/l/90 min, P = 0.05, respectively). In patients with Cushing's disease, galanin evoked a remarkable PRL rise with hormone levels which were significantly greater (P < 0.001) than those observed in the same patients after infusion of saline (21908 +/- 4180 vs 534 +/- 1556 mU/l/90 min) or after galanin administration in controls (P < 0.01). The PRL response to TRH and, much more so, to metoclopramide was significantly lower in patients with Cushing's disease than in normal subjects (42125 +/- 8000 vs 73181 +/- 7246 mU/l/90 min, P < 0.01 after TRH and 79095 +/- 27265 vs 229049 +/- 10602 mU/l/90 min, P < 0.01 after metoclopramide).
Galanin appears to be a specific, though weak, PRL secretagogue in normal subjects. The galanin-induced PRL release was significantly increased in patients with Cushing's disease. A number of hypothetical mechanisms may underlie the enhanced PRL reactivity to galanin in Cushing's disease. This finding together with the impaired PRL responsiveness to TRH and metoclopramide, also observed in this study, is a further example of a dysregulation of PRL secretion in patients with Cushing's disease.
人们认为甘丙肽在大鼠催乳素（PRL）分泌的调控中发挥作用。在人类中，这种作用尚不确定，因为促肾上腺皮质激素细胞会表达这种神经肽。然而，在促肾上腺皮质激素（ACTH）分泌增强的临床情况下，常常会观察到PRL水平升高。因此，我们评估了向库欣病患者和对照受试者输注甘丙肽对血清PRL水平的影响。为作比较，还在同一批患者中研究了PRL对促甲状腺激素释放激素（TRH）和甲氧氯普胺的反应。
进行了四项试验：（a）以0.3微克/千克/分钟的速度输注甘丙肽40分钟；（b）仅输注生理盐水；（c）甲氧氯普胺试验（静脉推注10毫克）；（d）TRH试验（静脉推注200毫克）。
对24名正常受试者和9名患有活动性库欣病的患者进行了研究。
通过放射免疫分析法对给药或输注生理盐水前及给药后90分钟采集的血样进行PRL血清浓度测定。
正常受试者和库欣病患者的血清PRL基线水平相当。在正常受试者中，与输注生理盐水相比，输注甘丙肽可使PRL明显升高（平均±标准误增加面积分别为6514±2572与540±571毫国际单位/升/90分钟，P = 0.05）。在库欣病患者中，甘丙肽可引起显著的PRL升高，其激素水平显著高于（P < 0.001）这些患者输注生理盐水后（21908±4180与534±1556毫国际单位/升/90分钟）或对照组输注甘丙肽后（P < 0.01）的水平。库欣病患者对TRH以及更明显地对甲氧氯普胺的PRL反应明显低于正常受试者（TRH后为42125±8000与73181±7246毫国际单位/升/90分钟，P < 0.01；甲氧氯普胺后为79095±27265与229049±10602毫国际单位/升/90分钟，P < 0.01）。
在正常受试者中，甘丙肽似乎是一种特异性的、但作用较弱的PRL促分泌素。在库欣病患者中，甘丙肽诱导的PRL释放显著增加。库欣病患者对甘丙肽的PRL反应性增强可能有多种潜在机制。本研究中还观察到的对TRH和甲氧氯普胺的PRL反应受损，是库欣病患者PRL分泌失调的又一实例。
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