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Giuseppe Riezzo [1] and Guglielmina Chimienti [2] and Caterina Clemente [1] and Benedetta D’Attoma [1] and Antonella Orlando [1] and Caterina Mammone Rinaldi [3] and Francesco Russo [1]

Academic Editor: Toshimi Chiba

1, Laboratory of Nutritional Pathophysiology, National Institute of Digestive Diseases, IRCCS “Saverio de Bellis”, Castellana Grotte, Bari, Italy, irccsdebellis.it

2, Department of Biosciences, Biotechnology and Biopharmaceutics, University of Bari, Bari, Italy, uniba.it

3, Department of Radiology and Imaging, National Institute of Digestive Diseases, IRCCS “Saverio de Bellis”, Castellana Grotte, Bari, Italy, irccsdebellis.it

Received Mar 22, 2017; Revised Jul 7, 2017; Accepted Aug 2, 2017

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Introduction

Functional constipation is a multifactorial disease very frequent among Europeans with an estimated prevalence of 17.1% [1]. In order to obtain a standardized definition of functional constipation, the Rome criteria (Rome I–IV) [2] have been developed and proposed, even though they are currently used for research purposes, mainly in clinical trials.

Functional constipation is thought to be the result of several causes including diet low in fibre content, autonomic neuropathy, disorders of the enteric nervous system, and alterations in the profile of circulating gastrointestinal (GI) peptides. A proposed classification of constipation according to the colonic transit time categorized patients as having “slow transit constipation” (STC) or “normal transit constipation” (NTC) [3]. STC seems to be caused by impaired colonic motility; even if it has also been observed that dysmotility disorders in these patients are not limited to the gut but, rather, they extend to other GI tracts such as esophagus, stomach, small bowel, gallbladder, and anorectum [4]. These data have suggested the involvement of a dysfunctional enteric nervous system, as already proposed as a cause of STC in subjects who have undergone pelvic surgery or have given birth [5]. The study of the neuroendocrine profile in STC patients had shown that a number of gut peptides, including motilin, corticotrophin-releasing factor (CRF), somatostatin, and neurotensin, may induce alterations of colonic motility [6–8]. In rabbits, motilin has been demonstrated to excite the colon through pathways different from those of cholinergic motor nerves [9] and, more recently, a research...
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
     
     
     
     
 

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