Colonic fermentation influences lower esophageal sphincter function in gastroesophageal reflux disease

被引:166
作者
Piche, T
Bruley, S
Des Varannes, SB
Sacher-Huvelin, S
Holst, JJ
Cuber, JC
Galmiche, JP [1 ]
机构
[1] CHU Hotel Dieu, CIC, INSERM, F-44093 Nantes 1, France
[2] CHU Hotel Dieu, U 539, F-44093 Nantes 1, France
[3] Univ Copenhagen, Panum Inst, Dept Med Physiol, DK-2200 Copenhagen N, Denmark
[4] Hop Edouard Herriot, INSERM, U 45, Lyon, France
关键词
D O I
10.1053/gast.2003.50159
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background & Aims: Colonic fermentation of carbohydrates is known to influence gastric and esophageal motility in healthy subjects. This study investigated the effects of colonic fermentation induced by oral administration of fructooligosaccharides (FOS) in patients with gastroesophageal reflux disease (GERD). Methods: In the cross-over design used in the study, 9 patients with symptomatic GERD were administered a low-residue diet (i.e., 10 g fiber/day) during 2, 7-day periods, receiving either 6.6 g of FOS or placebo 3 times daily after meals. Each period was separated by a wash out of at least 3 weeks. On day 7, esophageal motility and pH were recorded in fasting conditions and after a test meal containing 6.6 g of FOS or placebo. Breath hydrogen concentrations (reflecting colonic fermentation) and plasma concentrations of glucagon-like peptide 1 (GLP-1), peptide YY, and cholecystokinin were monitored. Results: Compared with placebo, FOS led to a significant increase in the number of transient lower esophageal sphincter relaxations (TLESRs) and reflux episodes, esophageal acid exposure, and the symptom score for GERD. The integrated plasma response of GLP-1 was significantly higher after FOS than placebo. Conclusions: Colonic fermentation of indigestible carbohydrates increases the rate of TLESRs, the number of acid reflux episodes, and the symptoms of GERD. Although different mechanisms are likely to be involved, excess release of GLP-1 may account, at least in part, for these effects.
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页码:894 / 902
页数:9
相关论文
共 41 条
[1]   EFFECTS OF PEPTIDE-YY AND NEUROPEPTIDE-Y ON GASTRIC-EMPTYING IN MAN [J].
ALLEN, JM ;
FITZPATRICK, ML ;
YEATS, JC ;
DARCY, K ;
ADRIAN, TE ;
BLOOM, SR .
DIGESTION, 1984, 30 (04) :255-262
[2]   INTESTINAL CONTROL OF GASTRIC TONE [J].
AZPIROZ, F ;
MALAGELADA, JR .
AMERICAN JOURNAL OF PHYSIOLOGY, 1985, 249 (04) :G501-G509
[3]   VAGALLY MEDIATED GASTRIC RELAXATION INDUCED BY INTESTINAL NUTRIENTS IN THE DOG [J].
AZPIROZ, F ;
MALAGELADA, JR .
AMERICAN JOURNAL OF PHYSIOLOGY, 1986, 251 (06) :G727-G735
[4]   CHOLECYSTOKININ AND NITRIC-OXIDE IN TRANSIENT LOWER ESOPHAGEAL SPHINCTER RELAXATION TO GASTRIC DISTENSION IN DOGS [J].
BOULANT, J ;
FIORAMONTI, J ;
DAPOIGNY, M ;
BOMMELAER, G ;
BUENO, L .
GASTROENTEROLOGY, 1994, 107 (04) :1059-1066
[5]   Short-chain fatty acids modify colonic motility through nerves and polypeptide YY release in the rat [J].
Cherbut, C ;
Ferrier, L ;
Rozé, C ;
Anini, Y ;
Blottière, H ;
Lecannu, G ;
Galimiche, JP .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 1998, 275 (06) :G1415-G1422
[6]   Endogenous cholecystokinin enhances postprandial gastroesophageal reflux in humans through extrasphincteric receptors [J].
Clavé, P ;
González, A ;
Moreno, A ;
López, R ;
Farré, A ;
Cussó, X ;
D'Amato, M ;
Azpiroz, F ;
Lluís, F .
GASTROENTEROLOGY, 1998, 115 (03) :597-604
[7]  
CLOAREC D, 1991, GASTROEN CLIN BIOL, V15, P588
[8]  
Delgado-Aros S, 2002, AM J PHYSIOL-GASTR L, V282, pG424
[9]   MECHANISMS OF LOWER ESOPHAGEAL SPHINCTER INCOMPETENCE IN PATIENTS WITH SYMPTOMATIC GASTROESOPHAGEAL REFLUX [J].
DENT, J ;
HOLLOWAY, RH ;
TOOULI, J ;
DODDS, WJ .
GUT, 1988, 29 (08) :1020-1028
[10]   PEPTIDE YY-LIKE IMMUNOREACTIVITY IN THE CENTRAL-NERVOUS-SYSTEM OF THE RAT [J].
EKMAN, R ;
WAHLESTEDT, C ;
BOTTCHER, G ;
SUNDLER, F ;
HAKANSON, R ;
PANULA, P .
REGULATORY PEPTIDES, 1986, 16 (02) :157-168