Rapid gastric emptying, rather than delayed gastric emptying, might provoke functional dyspepsia
Rapid gastric emptying, rather than delayed gastric emptying, might provoke functional dyspepsia
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DOI：
10.1111/j.1440-1746.2011.06627.x
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发表时间：
2011-04-01
影响因子：
4.1
通讯作者：
Mori, Masatomo
中科院分区：
文献类型：
--
作者：
Kusano, Motoyasu;Zai, Hiroaki;Mori, Masatomo
已经表明FD患者中可能存在三种可能的胃功能障碍机制：（i）胃排空延迟，（ii）食物摄入的胃调节受损，和（iii）对胃扩张的超敏反应。餐后饱胀感似乎是报告餐后症状加重的患者中最严重的症状。因此，人们一直认为，延迟胃排空和随之而来的长期胃窦扩张可以减少饥饿，增加饱腹感，甚至引起胃部不适，所有这些都将构成一个显着的障碍，以充分nutrition.We以前报道，餐后饮水抑制胃窦运动沿着胆囊收缩素（CCK）在正常受试者。我们认为，CCK的快速增加后，水的摄入量是由相关的反馈机制，脂肪食糜流入到十二指肠，抑制胃窦活动。这种十二指肠-胃的相互作用被称为“十二指肠破裂”。“我们还报道了摄入高粘度液体餐后的总胃排空比低粘度餐后更快，因为低粘度液体餐在快速流入十二指肠后抑制胃排空。考虑到这些结果，我们假设快速胃排空而不是延迟胃排空可能是FD的原因。在某些餐后窘迫综合征（PDS）患者中，我们发现PDS相关的消化不良与餐后早期胃排空加快之间存在显著的对应关系，值得强调的是，十二指肠和十二指肠-胃相互作用（十二指肠破裂）可能在FD的病理生理学中起重要作用。我们认为，在FD患者中，胃快速排空可能比胃排空延迟更重要。
It has been suggested that there could be three possible mechanisms of gastric dysfunction in patients with FD: (i) delayed gastric emptying, (ii) impaired gastric accommodation of food intake, and (iii) hypersensitivity to gastric distention. Postprandial fullness seems to be the most severe symptom in patients who report aggravation of their symptoms after meals. Therefore, it has been assumed that delayed gastric emptying and consequent prolonged antral distension could reduce hunger, increase satiety, and even cause gastric discomfort, all of which would pose a significant barrier to adequate nutrition.We previously reported that postprandial water intake inhibits gastric antral motility along with an increase of cholecystokinin (CCK) in normal subjects. We assumed that the rapid increase of CCK after water intake was initiated by a feedback mechanism related to the inflow of fatty chyme into the duodenum that inhibits gastric antral activity. This duodeno-gastric interaction is known as the "duodenal break." We also reported that total gastric emptying was more rapid after the intake of a high-viscosity liquid meal than after a low-viscosity meal, because the low-viscosity liquid meal inhibits gastric empting after rapid initial inflow into the duodenum.Considering these results, we hypothesized that rapid gastric emptying, rather than delayed gastric emptying, could be a cause of FD. In some patients with postprandial distress syndrome (PDS), we have found a significant correspondence between PDS-related dyspepsia and accelerated gastric emptying in the early postprandial period.It is worth emphasizing that the duodenum and the duodeno-gastric interaction (duodenal break) could have an important role in the pathophysiology of FD. We consider that rapid gastric emptying might be a more important factor than delayed gastric emptying in patients with FD.