GERD and obesity: is the autonomic nervous system the missing link?
GERD and obesity: is the autonomic nervous system the missing link?
复制标题
胃食管反流病和肥胖：自主神经系统是缺失的一环吗？
DOI：
10.1615/critrevbiomedeng.2014011035
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发表时间：
2014
影响因子：
--
通讯作者：
Markad V. Kamath
中科院分区：
文献类型：
--
作者：
Neranjani Devendran;Nita Chauhan;David Armstrong;A. R. Upton;Markad V. Kamath
胃食管反流病（GERD）是一种常见的慢性疾病，不仅会损害受其影响的人的生活质量，而且还会造成重大的经济负担。由于胃内容物进入食道，它包括广泛的症状。除了食管裂孔疝之外，GERD最常见的原因被认为是短暂的下食管括约肌松弛。下食管括约肌（LES）通常具有比胃更高的静息张力，从而防止胃内容物回流到食管中。GERD和GERD症状在肥胖个体中的更高患病率产生了对理解这两种状况与潜在生理机制之间的关联的极大兴趣。然而，GERD和肥胖之间的潜在关系以及肥胖可能导致反流的确切机制仍然不确定。已经提出GERD患者的自主神经功能改变，更具体地说，副交感神经活动减少。肥胖的个体也表现出副交感神经活动减少，这可能在通过运动、饮食控制和减肥手术减轻体重后逆转。由于LES的收缩和舒张是迷走神经介导的，因此出现的问题是自主神经系统是否是肥胖和GERD之间缺失的环节。在这篇文章中，我们检查了目前的证据，并假设交感迷走神经刺激LES的潜在不平衡是肥胖个体GERD症状患病率增加的关键因素。
Gastroesophageal reflux disease (GERD) is a common chronic condition that not only impairs the quality of life of those who are affected by it but also poses a significant economic burden. It encompasses a wide spectrum of symptoms as a result of gastric content moving into the esophagus. The most common cause of GERD, other than a hiatus hernia, is considered to be transient lower esophageal sphincter relaxation. The lower esophageal sphincter (LES) normally has a higher resting tone than the stomach, thus preventing the reflux of gastric contents into the esophagus. The greater prevalence of GERD and GERD symptoms in obese individuals has generated significant interest in understanding the association between these 2 conditions and the underlying physiological mechanisms. The potential relationship between GERD and obesity and the exact mechanism by which obesity may cause reflux, however, remains uncertain. It has been proposed that patients with GERD have altered autonomic nervous function and, more specifically, have reduced parasympathetic activity. Obese individuals also have shown diminished parasympathetic activity, which may be reversed after weight reduction through exercise, diet control, and bariatric surgery. Given that contraction and relaxation of the LES are vagally mediated, the question that arises is whether the autonomic nervous system is, in fact, the missing link between obesity and GERD. In this article we examine the current evidence and hypothesize that the potential imbalance in sympathovagal stimulation to the LES is a key contributing factor to the increased prevalence of GERD symptoms in obese individuals.