Obesity does not increase effects of synthetic ghrelin on human gastric motor functions
Obesity does not increase effects of synthetic ghrelin on human gastric motor functions
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DOI：
10.1053/j.gastro.2006.09.021
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发表时间：
2006-11-01
期刊：
影响因子：
29.4
通讯作者：
Zinsmeister, Alan R.
中科院分区：
文献类型：
--
作者：
Cremonini, Filippo;Camilleri, Michael;Zinsmeister, Alan R.
目的：胃促生长素由胃分泌，刺激食物摄入。肥胖个体空腹血浆胃饥饿素水平较低，但食欲增加，表明肥胖对内源性胃饥饿素的反应更大。本研究的目的是比较外源性胃饥饿素（刺激生长激素[GH]在生理范围内释放的剂量）与安慰剂对胃排空、胃容量和餐后症状的影响，并确定体重（从正常体重到肥胖）是否影响对胃饥饿素的反应。方法：静脉注射合成人胃促生长素（0.33 μ g/kg）或生理盐水后，采用tc -99m单光子发射计算机断层扫描和闪烁成像（In-111蛋粉，300 kcal）联合测量血浆GH、胃容量和胃排空，并使用视觉模拟量表测量餐后症状。结果：在25名肥胖受试者（男性5名，女性20名；体重指数[BMI]， 36 +/- 4 kg/m(2)）和13名年龄相近的正常体重女性（BMI, 22 +/- 2 kg/m(2)）中，与安慰剂相比，胃饥饿素在注射后40分钟提高生长激素水平（15.0 +/- 2.4 ng/mL），并有减少空腹胃容量的趋势（P= 0.059）。BMI对治疗反应没有影响，胃饥饿素和生理盐水对餐后（P= 0.09）或（餐后减去禁食）胃容量、胃排空或餐后综合症状的变化也没有差异。饥饿素的作用在肥胖和正常体重的参与者之间没有差异。结论：在以女性为主的队列中，在刺激生长素生理性血浆水平的剂量下，合成胃饥饿素倾向于减少空腹胃容量，而不改变餐后胃容量或胃排空。这些数据与高体重与胃对胃促生长素的反应性增加有关的假设不一致。
Aims: Ghrelin is secreted by the stomach and stimulates food intake. Obese individuals have lower fasting plasma ghrelin levels but increased appetite, suggesting greater responses to endogenous ghrelin in obesity. The aim of this study was to compare effects of exogenous ghrelin (at a dose that stimulates growth hormone [GH] release in the physiologic range) versus placebo on gastric emptying, gastric volume, and postprandial symptoms and determine whether body mass (ranging from normal weight to obesity) influences responses to ghrelin. Methods: After intravenous bolus synthetic human ghrelin (0.33 mu g/kg) or saline, we measured plasma GH, gastric Volume, and gastric emptying by combined Tc-99m-single-photon emission computed tomography and scintigraphy (In-111 egg meal, 300 kcal) and postprandial symptoms using visual analogue scales. Results: In 25 obese Subjects (S men and 20 women; body mass index [BMI], 36 +/- 4 kg/m(2)) and 13 female normal-weight (BMI, 22 +/- 2 kg/m(2)) subjects of similar ages, ghrelin increased GH levels (15.0 +/- 2.4 ng/mL) at 40 minutes postinjection and tended to decrease fasting gastric volumes compared with placebo (P=.059). There were no effects of BMI on treatment response and no differences between ghrelin and saline on postprandial (P=.09) or change in (postprandial minus fasting) gastric volumes, gastric emptying, or aggregate postprandial symptoms. Effects of ghrelin did not differ between obese and normal-weight participants. Conclusions: At doses that stimulate physiologic GH plasma levels, synthetic ghrelin tended to decrease fasting gastric volumes without altering postprandial volumes or gastric emptying in a predominantly female cohort. The data are not consistent with the hypothesis that higher body mass is associated with increased gastric responsiveness to ghrelin.