Mushref Mazen Al, Srinivasan Shanthi
Division of Digestive Diseases, Emory University, 615 Michael Street, Atlanta, GA 30322, and Atlanta VA Medical Center, Decatur, GA, USA.
Ann Transl Med. 2013 Jul 1;1(2):14. doi: 10.3978/j.issn.2305-5839.2012.11.01.
Obesity is highly prevalent worldwide and is associated with significant morbidity and mortality. The focus of this review is to delineate the changes in gastrointestinal motility observed in obesity. A systematic review of the published literature on obesity and gastrointestinal motility was performed. Here, we describe the current understanding of the changes in obesity in the esophagus, stomach, small intestine and colon. Major findings include supportive evidence for increased gastroesophageal reflux disease and esophageal motility disorders in obesity, and a rapid gastric emptying time seen in obese individuals. The proximal small intestinal transit seems to be increased in obesity and this may be secondary to efficient nutrient absorption and subsequent lack of nutrient-induced satiety signals conveyed from the small intestine. In obesity, there is some evidence for delayed colonic transit as well as a reduction in colonic serotonin availability. The molecular mechanisms underlying altered motility in obesity could be secondary to reduced cannabinoids or its receptor cannabinoid receptor 1 (CB1) expression as well as due to loss of neuronal nitric oxide synthase (nNOS) neurons. The interactions of diet and obesity and the alteration of microbiota in this setting are just being explored and may offer novel insights into the changes of gastrointestinal motility in obesity.
肥胖在全球范围内高度流行,且与显著的发病率和死亡率相关。本综述的重点是阐述肥胖时观察到的胃肠动力变化。我们对已发表的关于肥胖与胃肠动力的文献进行了系统综述。在此,我们描述了目前对肥胖时食管、胃、小肠和结肠变化的认识。主要发现包括肥胖中胃食管反流病和食管动力障碍增加的支持性证据,以及肥胖个体胃排空时间加快。肥胖时近端小肠转运似乎增加,这可能继发于有效的营养吸收以及随后小肠缺乏营养诱导的饱腹感信号传递。在肥胖中,有证据表明结肠转运延迟以及结肠5-羟色胺可用性降低。肥胖时动力改变的分子机制可能继发于大麻素或其受体大麻素受体1(CB1)表达降低,以及神经元型一氧化氮合酶(nNOS)神经元的丧失。在这种情况下,饮食与肥胖的相互作用以及微生物群的改变刚刚开始被探索,可能为肥胖时胃肠动力的变化提供新的见解。