Implantable gastric stimulator does not prevent the increase in plasma ghrelin levels that occurs with weight loss.
Implantable gastric stimulator does not prevent the increase in plasma ghrelin levels that occurs with weight loss.
复制标题
植入式胃刺激器不能阻止体重减轻时血浆生长素释放肽水平的增加。
DOI：
10.1038/oby.2010.162
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Aronne,LouisJ
中科院分区：
文献类型：
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作者：
Korner,Judith;Nandi,Anindita;Wright,SuzanneM;Waitman,Jonathan;McMahon,DonaldJ;Bessler,Marc;Aronne,LouisJ
SHAPE（筛查健康评估和起搏器评价）试验是一项为期24个月的随机多中心安慰剂对照研究，旨在确定植入式胃刺激器（IGS）减肥的疗效。本报告是一项研究者发起的子研究，在一个研究中心进行，旨在评估IGS是否影响ghrelin和肽YY（PYY）的血浆水平。在所有受试者中植入了该器械，但在前12个月期间，治疗组（n= 7，BMI = 41.5 ± 2.0 kg/m2）中激活了该器械，对照组（n= 6，BMI = 39.5 ± 1.7 kg/m2）中未激活该器械。在12-24个月期间，两组中的IGS都被激活。在第0、12和24个月抽取空腹静脉血，并在第12个月进行口服葡萄糖耐量试验（OGTT）。虽然在6个月时体重减轻没有差异（对照组：−6.6 ± 1.5% vs.治疗组：−6.2 ± 1.4%），但在24个月时，对照组表现出较基线的体重增加（+2.2 ± 1.5%），与治疗组的体重减轻（−1.9 ± 1.4%;P< 0.05）存在显著差异。在12个月时，治疗组的空腹ghrelin显著增加（P< 0.05）（285 ± 35至336 ± 35 pg/ml;体重变化，−4.9 ± 1.4%），但对照组没有（211 ± 36至208 ± 35 pg/ml;体重变化，−3.4 ± 1.5%）。餐后血浆ghrelin抑制或空腹和餐后PYY水平无显著变化。总之，IGS不能阻止与体重减轻相关的空腹血浆ghrelin水平的增加。需要进一步的研究来确定技术的变化是否可以改善减肥和维持，也许可以使用肠道激素作为可能有效的生物标志物。
The SHAPE (Screened Health Assessment and Pacer Evaluation) trial was a 24 month randomized multicenter placebo‐controlled study to determine the efficacy of an implantable gastric stimulator (IGS) for weight loss. This report is an investigator‐initiated sub‐study at one site designed to assess whether IGS affects plasma levels of ghrelin and peptide YY (PYY). The device was implanted in all subjects but was activated in the Treatment group (n= 7, BMI = 41.5 ± 2.0 kg/m2) and remained inactive in the Control (n= 6, BMI = 39.5 ± 1.7 kg/m2) during the first 12 months. IGS was activated in both groups during months 12–24. Fasting venous blood was drawn at months 0, 12, and 24 and an oral glucose tolerance test (OGTT) was performed at month 12. Although there was no difference in weight loss at 6 months (Control: −6.6 ± 1.5% vs. Treatment: −6.2 ± 1.4%), at 24 months the Control group exhibited weight gain from baseline (+2.2 ± 1.5%) that was significantly different from the weight loss in the Treatment group (−1.9 ± 1.4%;P< 0.05). At 12 months, fasting ghrelin was significantly increased (P< 0.05) in the Treatment group (285 ± 35 to 336 ± 35 pg/ml; weight change, −4.9 ± 1.4%), but not in the Control (211 ± 36 to 208 ± 35 pg/ml; weight change, −3.4 ± 1.5%). No significant change was observed in postprandial suppression of plasma ghrelin or in fasting and postprandial PYY levels. In conclusion, IGS does not prevent the increase in fasting plasma ghrelin levels associated with weight loss. Further studies are needed to determine whether changes in technology can improve weight loss and maintenance, perhaps using gut hormones as biomarkers of possible efficacy.