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BioMed Research International
Volume 2018 (2018), Article ID 9171905, 13 pages
Review Article

Functions and Signaling Pathways of Amino Acids in Intestinal Inflammation

1College of Animal Science and Technology, Southwest University, Chongqing 400716, China
2College of Animal Science, South China Agricultural University, Guangzhou 510642, China
3College of Veterinary Medicine, Yangzhou University, 48 Wenhui East Road, Yangzhou, Jiangsu 225009, China

Correspondence should be addressed to Wenkai Ren and Yuanyi Peng

Received 30 September 2017; Revised 30 November 2017; Accepted 13 December 2017; Published 26 February 2018

Academic Editor: Lidong Zhai

Copyright © 2018 Fang He et al. 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.


Intestine is always exposed to external environment and intestinal microorganism; thus it is more sensitive to dysfunction and dysbiosis, leading to intestinal inflammation, such as inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), and diarrhea. An increasing number of studies indicate that dietary amino acids play significant roles in preventing and treating intestinal inflammation. The review aims to summarize the functions and signaling mechanisms of amino acids in intestinal inflammation. Amino acids, including essential amino acids (EAAs), conditionally essential amino acids (CEAAs), and nonessential amino acids (NEAAs), improve the functions of intestinal barrier and expressions of anti-inflammatory cytokines and tight junction proteins but decrease oxidative stress and the apoptosis of enterocytes as well as the expressions of proinflammatory cytokines in the intestinal inflammation. The functions of amino acids are associated with various signaling pathways, including mechanistic target of rapamycin (mTOR), inducible nitric oxide synthase (iNOS), calcium-sensing receptor (CaSR), nuclear factor-kappa-B (NF-κB), mitogen-activated protein kinase (MAPK), nuclear erythroid-related factor 2 (Nrf2), general controlled nonrepressed kinase 2 (GCN2), and angiotensin-converting enzyme 2 (ACE2).