ARGININE STIMULATES GROWTH-HORMONE SECRETION BY SUPPRESSING ENDOGENOUS SOMATOSTATIN SECRETION
ARGININE STIMULATES GROWTH-HORMONE SECRETION BY SUPPRESSING ENDOGENOUS SOMATOSTATIN SECRETION
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DOI：
10.1210/jcem-67-6-1186
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发表时间：
1988-12-01
影响因子：
5.8
通讯作者：
VONWERDER, K
中科院分区：
文献类型：
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作者：
ALBAROTH, J;MULLER, OA;VONWERDER, K
为了确定精氨酸（Arg）如何刺激GH分泌，我们研究了其与GHRH在体内和体外的相互作用。在四种情况下研究六名正常人：1）Arg-TRH，在30分钟内在500 mL盐水中施用30 μ g精氨酸，随后注射200 μ g TRH：2）GHRH-Arg-TRH，在Arg输注之前立即静脉内推注100 μ g GHRH-（1-44），随后静脉内施用200 μ g TRH; 3）GHRH试验，100 μ g GHRH作为静脉推注给予;和4）TRH试验，200 μ g TRH作为静脉推注剂量给予。在每次输注开始前30分钟和输注开始后120分钟，每隔15分钟采集一次血样。将大鼠垂体前叶细胞与精氨酸（3、6、15、30和60 mg/mL）和GHRH（0.05、1、5和10 nmol/L）共孵育3 h。在培养基中测定大鼠GH。Arg-TRH后，平均血清GH浓度显著增加，从0.6增加到23.3 ±。7.3 (.+-. TRH使血清TSH和PRL显著增加（最大TSH，11.1 ± 0.001 μ g/L）。1.8 mU/L;最大PRL，74.6 ±。8.4μ g/L）。在GHRH-Arg-TRH之后，最大血清GH水平显著更高（72.7 ± 0.01）。13.4而血清TSH和PRL增加到可比较的水平（TSH，10.2 ± 0.5 μ g/L）。3.0 mU/L; PRL为64.4 ±。13.6μ g/L）。单独的GHRH使血清GH增加至44.9 ± 0.01。9.8μ g/l显著低于单独给予GHRH、Arg和TRH时的剂量，使血清TSH增加至6.6 ± 0.5 μ g/l。0.6 mU/L，显著低于TSH对Arg-TRH的反应。仅TRH后的PRL增加也较低（47.2 ± 0.01）。6.8μ g/L）比Arg-TRH后的PRL反应。在体外精氨酸对基础和GHRH刺激的GH分泌没有影响。我们的研究结果表明，精氨酸与GHRH管理导致更高的血清GH水平比没有最大刺激剂量的GHRH或精氨酸单独。血清TSH对Arg-TRH的反应也大于单独对TRH的反应。我们的结论是，精氨酸的刺激作用是通过抑制内源性生长抑素分泌介导的。
To determine how arginine (Arg) stimulates GH secretion, we investigated its interaction with GHRH in vivo and in vitro. Six normal men were studied on four occasions: 1) Arg-TRH, 30 g arginine were administered in 500 mL saline in 30 min, followed by an injection of 200 .mu.g TRH: 2) GHRH-Arg-TRH, 100 .mu.g GHRH-(1-44) were given iv as a bolus immediately before the Arg infusion, followed by 200 .mu.g TRH, iv; 3) GHRH test, 100 .mu.g GHRH were given as an iv bolus; and 4) TRH test, 200 .mu.g TRH were given iv as a bolus dose. Blood samples were collected at 15-min intervals for 30 min before and 120 min after the start of each infusion. Anterior pituitary cells from rats were coincubated with Arg (3, 6, 15, 30, and 60 mg/mL) and GHRH (0.05, 1, 5, and 10 nmol/L) for a period of 3 h. Rat GH was measured in the medium. After Arg-TRH the mean serum GH concentration increased significantly from 0.6 to 23.3 .+-. 7.3 (.+-. SE) .mu.g/L at 60 min. TRH increased serum TSH and PRL significantly (maximum TSH, 11.1 .+-. 1.8 mU/L; maximum PRL, 74.6 .+-. 8.4 .mu.g/L). After GHRH-Arg-TRH, the maximal serum GH level was significantly higher (72.7 .+-. 13.4 .mu.g/L) than that after Arg-TRH alone, whereas serum TSH and PRL increased to comparable levels (TSH, 10.2 .+-. 3.0 mU/L; PRL, 64.4 .+-. 13.6 .mu.g/L). GHRH alone increased serum GH to 44.9 .+-. 9.8 .mu.g/l significantly less than when GHRH, Arg, and TRH were given TRH alone increased serum TSH to 6.6 .+-. 0.6 mU/L, significantly less than the TSH response to Arg-TRH. The PRL increase after TRH only also was lower (47.2 .+-. 6.8 .mu.g/L) than the PRL response after Arg-TRH. In vitro Arg had no effect on basal and GHRH-stimulated GH secretion. Our results indicate that Arg administered with GHRH led to higher serum GH levels than did a maximally stimulatory dose of GHRH or Arg alone. The serum TSH response to Arg-TRH also was greater than that to TRH alone. We conclude that the stimulatory effects of Arg are mediated by suppression of endogenous somatostatin secretion.