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首页> 外文期刊>American Journal of Physiology >Postprandial gut hormone responses and glucose metabolism in cholecystectomized patients
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Postprandial gut hormone responses and glucose metabolism in cholecystectomized patients

机译：胆囊切除术患者的餐后肠道激素反应和葡萄糖代谢

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Preclinical studies suggest that gallbladder emptying, via bile acid-induced activation of the G protein-coupled receptor TGR5 in intestinal L cells, may play a significant role in the secretion of the incretin hormone glucagon-like peptide-1 (GLP-1) and, hence, postprandial glucose homeostasis. We examined the secretion of gut hormones in cholecystectomized subjects to test the hypothesis that gallbladder emptying potentiates postprandial release of GLP-1. Ten cholecystectomized subjects and 10 healthy, age-, gender-, and body mass index-matched control subjects received a standardized fat-rich liquid meal (2,200 kJ). Basal and postprandial plasma concentrations of glucose, insulin, C-peptide, glucagon, GLP-1, glucose-dependent insulinotropic polypeptide (GBP), glucagon-like peptide-2 (GLP-2), cholecystokinin (CCK), and gastrin were measured. Furthermore, gastric emptying and duodenal and serum bile acids were measured. We found similar basal glucose concentrations in the two groups, whereas cholecystectomized subjects had elevated postprandial glucose excursions. Cholecystectomized subjects had reduced postprandial concentrations of duodenal bile acids, but preserved postprandial plasma GLP-1 responses, compared with control subjects. Also, cholecystectomized patients exhibited augmented fasting glucagon. Basal plasma CCK concentrations were lower and peak concentrations were higher in cholecystectomized patients. The concentrations of GIP, GLP-2, and gastrin were similar in the two groups. In conclusion, cholecystectomized subjects had preserved postprandial GLP-1 responses in spite of decreased duodenal bile delivery, suggesting that gallbladder emptying is not a prerequisite for GLP-1 release. Cholecystectomized patients demonstrated a slight deterioration of postprandial glycemic control, probably because of metabolic changes unrelated to incretin secretion.
机译：临床前研究表明，胆汁排空是通过胆汁酸诱导的肠道L细胞中G蛋白偶联受体TGR5的活化，在肠降血糖素激素胰高血糖素样肽1（GLP-1）和，因此，餐后葡萄糖体内平衡。我们检查了胆囊切除的受试者中肠道激素的分泌，以检验胆囊排空增强餐后GLP-1释放的假说。 10名胆囊切除术受试者和10名健康，年龄，性别和体重指数匹配的对照受试者接受了标准的富含脂肪的流质餐（2,200 kJ）。测量了基础和餐后血浆葡萄糖，胰岛素，C肽，胰高血糖素，GLP-1，葡萄糖依赖性促胰岛素多肽（GBP），胰高血糖素样肽2（GLP-2），胆囊收缩素（CCK）和胃泌素的浓度。此外，还测量了胃排空，十二指肠和血清胆汁酸。我们发现两组中的基础葡萄糖浓度相似，而经胆囊切除术的受试者餐后葡萄糖偏移升高。与对照组相比，经胆囊切除术的受试者餐后十二指肠胆汁酸浓度降低，但保留了餐后血浆GLP-1反应。此外，经胆囊切除术的患者表现出增强的禁食胰高血糖素。胆囊切除术患者的基础血浆CCK浓度较低，峰值浓度较高。两组中GIP，GLP-2和胃泌素的浓度相似。总之，尽管十二指肠胆汁递送减少，但经胆囊切除术的受试者仍保留了餐后GLP-1反应，这表明胆囊排空并不是GLP-1释放的前提。接受胆囊切除术的患者餐后血糖控制略有恶化，可能是由于与肠降血糖素分泌无关的代谢变化。

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