Roux-en-Y gastric bypass alters small intestine glutamine transport in the obese Zucker rat.
Roux-en-Y gastric bypass alters small intestine glutamine transport in the obese Zucker rat.
复制标题
Roux-en-Y 胃绕道术改变了肥胖 Zucker 大鼠的小肠谷氨酰胺转运。
DOI：
10.1152/ajpgi.00104.2009
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发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Cooney,RobertN
中科院分区：
文献类型：
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作者：
Wolff,BrynnS;Meirelles,Katia;Meng,Qinghe;Pan,Ming;Cooney,RobertN
Roux-en-Y胃旁路术（RYGB）的代谢效应是由术后胃肠道解剖结构的变化引起的，这些变化影响了肠道功能。谷氨酰胺是一种重要的肠道营养素，作为肠道新生的底物，参与调节葡萄糖代谢。本研究探讨了肥胖和RYGB对肠道谷氨酰胺转运和代谢的影响。首先，比较瘦和肥胖Zucker大鼠（ZRs）。然后研究RYGB和假手术对肥胖ZRs的影响。在术后第28天，收集小肠段（胆胰支、Roux支和共同通道）粘膜，分离刷状缘膜囊泡（BBMV）。测定谷氨酰胺转运蛋白活性和丰度、B 0AT 1蛋白和mRNA水平。测定谷氨酰胺酶、胞质磷酸烯醇式丙酮酸羧激酶（PEPCK-C）和葡萄糖-6-磷酸酶（G6 β）的水平，以评估谷氨酰胺代谢和肠道新生。肥胖增加了整个肠道的谷氨酰胺转运和B 0AT 1表达。RYGB增加胆胰管（3.8倍）和Roux肢（1.4倍）的谷氨酰胺转运活性，但对共同通道没有影响。RYGB后胆胰管分支和Roux分支中B 0AT 1 mRNA和蛋白的相对丰度分别增加6倍和10倍（P< 0.05 vs. PF），但共同通道中B 0AT 1 mRNA和蛋白的相对丰度没有增加。谷氨酰胺酶水平增加，而PEPCK-C和G6 β的相对丰度在RYGB后的所有肠段中降低。RYGB选择性增加谷氨酰胺吸收胆胰和Roux肢体的机制，涉及增加B 0AT 1的表达。RYGB后转氨酶水平增加，但PEPCK-C和G6 β的减少表明RYGB下调肠道新生。
The metabolic effects of Roux-en-Y gastric bypass (RYGB) are caused by postsurgical changes in gastrointestinal anatomy affecting gut function. Glutamine is a critical gut nutrient implicated in regulating glucose metabolism as a substrate for intestinal gluconeogenesis. The present study examines the effects of obesity and RYGB on intestinal glutamine transport and metabolism. First, lean and obese Zucker rats (ZRs) were compared. Then the effects of RYGB and sham surgery with pair feeding (PF) in obese ZRs were studied. Segments of small intestine (biliopancreatic limb, Roux limb, and common channel) mucosa were harvested and brush border membrane vesicles (BBMVs) were isolated onpostoperative day 28. Glutamine transporter activity and abundance, B0AT1 protein, and mRNA levels were measured. Levels of glutaminase, cytosolic phosphoenolpyruvate carboxykinase (PEPCK-C), and glucose-6-phosphatase (G6Pase) were measured to assess glutamine metabolism and intestinal gluconeogenesis. Obesity increased glutamine transport and B0AT1 expression throughout the intestine. RYGB increased glutamine transport activity in the biliopancreatic (3.8-fold) and Roux limbs (1.4-fold) but had no effect on the common channel. The relative abundance of B0AT1 mRNA and protein were increased in the biliopancreatic (6-fold) and Roux limbs (10-fold) after RYGB (P< 0.05 vs. PF), but not the common channel. Glutaminase levels were increased, whereas the relative abundance of PEPCK-C and G6Pase were decreased in all segments of intestine after RYGB. RYGB selectively increased glutamine absorption in biliopancreatic and Roux limbs by a mechanism involving increased B0AT1 expression. Post-RYGB glutaminase levels were increased, but the reductions in PEPCK-C and G6Pase suggest that RYGB downregulates intestinal gluconeogenesis.