Herrmann C, Göke R, Richter G, Fehmann H C, Arnold R, Göke B
Department of Internal Medicine, Philipps University of Marburg, Germany.
Digestion. 1995;56(2):117-26. doi: 10.1159/000201231.
The nutrient-dependent glucagon-like peptide-1 (7-36) amide (GLP-1) release was studied in comparison to the glucose-dependent insulin-releasing polypeptide (GIP) response in 10 healthy volunteers each undergoing various protocols. Plasma samples were saved up to 120 min after challenges by oral, intravenous or intraduodenal administration of nutrients. Basal plasma-GLP-1 concentrations ranged between 0.4 and 1.4 pM, maximal postprandial GLP-1 levels peaked between 10 and 12 pM. Intravenous glucose (25 g i.v.) did not change basal GLP-1 levels. Oral administration of glucose (50 g) induced a biphasic GLP-1 release peaking at 30-60 min and a biphasic GIP release peaking at 5 and 45 min. This increase paralleled the secretion of insulin. Oral galactose (100 g) and amino acids (25 g) also induced a rapid plasma GLP-1 response. After fat (67 g corn oil) a strong and long-lasting (> 120 min) increase of GLP-1 plasma levels occurred. When a mixed liquid meal was given (6 g soybean oil, 5 g casein, 13 g glucose) immunoreactive (IR)-GLP-1 rapidly increased and peaked after 5 min with declining levels after 30 min. In response to an intraduodenal infusion of a small glucose load (5.34 g within 120 min) a rapid, short-lasting GLP-1 response occurred whereas plasma GIP and insulin levels remained unaltered. Luminal perfusion of an isolated vascularly perfused rat ileum with a polydiet induced a rapid rise of portally released IR-GLP-1 which was followed by a sustained release. Glucose evoked sodium-dependently a sharp increase of IR-GLP-1 levels followed by a plateau release. The intraluminal infusion of a mixture of amino acids or fat was without any effect on IR-GLP-1. We hypothesize that in contrast to GIP the GLP-1 release from L cells is triggered by nervous reflexes, by putative humoral factor(s) being released from the upper small intestine in addition to nutrient stimuli acting at the luminal surface of the gut.
在10名健康志愿者中，分别采用不同方案，研究了营养物质依赖性胰高血糖素样肽-1（7-36）酰胺（GLP-1）的释放情况，并与葡萄糖依赖性胰岛素释放多肽（GIP）的反应进行了比较。在通过口服、静脉注射或十二指肠内给予营养物质进行刺激后，采集血浆样本长达120分钟。基础血浆GLP-1浓度在0.4至1.4 pM之间，餐后GLP-1最高水平在10至12 pM之间达到峰值。静脉注射葡萄糖（25 g静脉注射）未改变基础GLP-1水平。口服葡萄糖（50 g）诱导双相GLP-1释放，在30至60分钟达到峰值，以及双相GIP释放，在5分钟和45分钟达到峰值。这种增加与胰岛素分泌平行。口服半乳糖（100 g）和氨基酸（25 g）也诱导快速的血浆GLP-1反应。给予脂肪（67 g玉米油）后，血浆GLP-1水平出现强烈且持久（> 120分钟）的升高。给予混合液体餐（6 g大豆油、5 g酪蛋白、13 g葡萄糖）后，免疫反应性（IR）-GLP-1迅速升高，在5分钟后达到峰值，30分钟后水平下降。响应十二指肠内输注少量葡萄糖负荷（120分钟内5.34 g），出现快速、短暂的GLP-1反应，而血浆GIP和胰岛素水平保持不变。用多混合饮食对分离的血管灌注大鼠回肠进行腔内灌注，诱导门静脉释放的IR-GLP-1迅速升高，随后持续释放。葡萄糖以钠依赖性方式引起IR-GLP-1水平急剧升高，随后是平台期释放。腔内输注氨基酸或脂肪混合物对IR-GLP-1没有任何影响。我们推测，与GIP不同，L细胞释放GLP-1是由神经反射触发的，除了作用于肠腔表面的营养刺激外，还由来自小肠上段释放的假定体液因子触发。
