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胃排空对餐后胃饥饿素反应的影响。

Effects of gastric emptying on the postprandial ghrelin response.

作者信息

Blom Wendy A M, Lluch Anne, Vinoy Sophie, Stafleu Annette, van den Berg Robin, Holst Jens J, Kok Frans J, Hendriks Henk F J

机构信息

Department of Food and Chemical Risk Analysis, Netherlands Organization for Applied Scientific Research Quality of Life, Zeist, The Netherlands.

出版信息

Am J Physiol Endocrinol Metab. 2006 Feb;290(2):E389-95. doi: 10.1152/ajpendo.00238.2005. Epub 2005 Sep 27.

Abstract

Distension and chemosensitization of the stomach are insufficient to induce a ghrelin response, suggesting that postgastric feedback is required. This postgastric feedback may be regulated through insulin. We investigated the relation between gastric emptying rate and the postprandial ghrelin response as well as the role of insulin and other hormones possibly mediating this response. Fifteen healthy men [BMI 21.6 kg/m2 (SD 1.9), age 20.5 yr (SD 2.5)] were studied in a single-blind, crossover design. Subjects received two treatments separated by 1 wk: 1) a dairy breakfast in combination with a 3-h intravenous infusion of glucagon-like peptide-1 (GLP-1), which delays gastric emptying, and 2) a dairy breakfast in combination with a 3-h intravenous infusion of saline. Blood samples were drawn before breakfast and during the infusion. Postprandial ghrelin (total) responses were lower following the saline infusion compared with the GLP-1 infusion (P < 0.05). Acetaminophen concentrations, an indirect measurement of gastric emptying rate, were inversely correlated with total ghrelin concentrations (saline r = -0.76; 95% CI = -0.90, -0.49, GLP-1 r = -0.47; 95% CI = -0.76, -0.04). Ghrelin concentrations were only weakly correlated with insulin concentrations (saline r = -0.36; 95% CI = -0.69, 0.09; GLP- 1 r = -0.42; 95% CI = -0.73, 0.03), but strongly inversely correlated with GIP concentrations (saline r = -0.74; 95% CI= -0.89, -0.45; GLP-1 r = -0.63; 95% CI = -0.84, -0.27). In conclusion, our results support the hypothesis that ghrelin requires postgastric feedback, which may not be regulated through insulin. Conversely, our data suggest a role of glucose-dependent insulinotropic polypeptide in ghrelin secretion.

摘要

胃扩张和化学增敏不足以诱导胃饥饿素反应,这表明需要胃后反馈。这种胃后反馈可能通过胰岛素来调节。我们研究了胃排空率与餐后胃饥饿素反应之间的关系,以及胰岛素和其他可能介导这种反应的激素的作用。15名健康男性[体重指数21.6 kg/m²(标准差1.9),年龄20.5岁(标准差2.5)]采用单盲交叉设计进行研究。受试者接受两种间隔1周的治疗:1)一份乳制品早餐并静脉输注胰高血糖素样肽-1(GLP-1)3小时,这会延迟胃排空;2)一份乳制品早餐并静脉输注生理盐水3小时。在早餐前和输注期间采集血样。与输注GLP-1相比,输注生理盐水后餐后胃饥饿素(总量)反应较低(P<0.05)。对乙酰氨基酚浓度作为胃排空率的间接测量指标,与胃饥饿素总浓度呈负相关(生理盐水组r=-0.76;95%可信区间=-0.90,-0.49;GLP-1组r=-0.47;95%可信区间=-0.76,-0.04)。胃饥饿素浓度与胰岛素浓度仅呈弱相关(生理盐水组r=-0.36;95%可信区间=-0.69,0.09;GLP-1组r=-0.42;95%可信区间=-0.73,0.03),但与葡萄糖依赖性促胰岛素多肽浓度呈强负相关(生理盐水组r=-0.74;95%可信区间=-0.89,-0.45;GLP-1组r=-0.63;95%可信区间=-0.84,-0.27)。总之,我们的结果支持胃饥饿素需要胃后反馈这一假说,且这种反馈可能不受胰岛素调节。相反,我们的数据表明葡萄糖依赖性促胰岛素多肽在胃饥饿素分泌中起作用。

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