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Nutrients
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Nutrition, Gut Permeability, and Inflammation
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Nutrition, Gut Permeability, and Inflammation

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: closed (5 March 2024) | Viewed by 13732

Special Issue Editor

Prof. Dr. David H. St-Pierre

E-Mail Website
Guest Editor
1. Department of Exercise Sciences, Université du Québec à Montréal, Montréal, QC H3C 3P8, Canada
2. CHU Sainte-Justine Research Center, Montréal, QC H3T 1C4, Canada
Interests: gastrointestinal peptides; metabolism; chronic inflammation; gut microbiota; prebiotics; obesogenic diets; sports nutrition
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is my pleasure to announce the launch of a new Special Issue of the journal Nutrients entitled “Nutrition, Gut Permeability and Inflammation”. This topic should clarify some key aspects of the pathophysiology of the most prevalent chronic diseases. Within the last decade, important advances in microbiology and gastroenterology have depicted the importance of communication axes between the gut microbiome, the intestine, and key organs and tissues. These include the gut/brain, gut/liver, and gut/muscle axes. Work from different research groups has underlined the key role of nutrition in promoting the alteration of the gut microbial flora, intestinal permeability, a pro-oxidative state, and a chronic activation of inflammatory responses. This immune priming is strongly suggested to trigger the activation of a host of chronic conditions which could include cardiometabolic, neurodegenerative, autoimmune, psychiatric disorders, and even musculoskeletal dysfunctions. The present Special Issue will provide a combination of resourceful review articles and insightful original research articles to clarify the roles of nutrients, the gut microbial flora, gut permeability on distinct immune responses, and the resulting pathological outcomes.

Prof. Dr. David H. St-Pierre
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • nutrients
  • gut permeability
  • inflammation
  • chronic diseases

Published Papers (3 papers)

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Research

12 pages, 761 KiB  
Article
Changes in Tryptophan Metabolism on Serotonin and Kynurenine Pathways in Patients with Irritable Bowel Syndrome
by Cezary Chojnacki, Aleksandra Błońska, Paulina Konrad, Marcin Chojnacki, Marcin Podogrocki and Tomasz Poplawski
Nutrients 2023, 15(5), 1262; https://doi.org/10.3390/nu15051262 - 3 Mar 2023
Cited by 1 | Viewed by 2245
Abstract
(1) Background: L-tryptophan is a substrate for the synthesis of many biological compounds through the serotonin and kynurenine pathways. These compounds have a significant influence on gastrointestinal functions and mental processes. The aim of the study was to evaluate the urinary excretion of [...] Read more.
(1) Background: L-tryptophan is a substrate for the synthesis of many biological compounds through the serotonin and kynurenine pathways. These compounds have a significant influence on gastrointestinal functions and mental processes. The aim of the study was to evaluate the urinary excretion of selected tryptophan metabolites in patients with constipation-predominant and diarrhoea-predominant irritable bowel syndrome (IBS-C and IBS-D, respectively), related to somatic and mental symptoms. (2) Methods: 120 people were included in the study and three groups were distinguished, with 40 individuals each, including healthy subjects (controls), patients with IBS-C and patients with IBS-D. The Gastrointestinal Symptoms Rating Scale (GSRS-IBS) was used to assess the severity of abdominal symptoms. The Hamilton Anxiety Rating Scale (HAM-A) and Hamilton Depression Rating Scale (HAM-D) were used to evaluate the mental state of patients. Using liquid chromatography tandem mass spectrometry (LC-MS/MS), L-tryptophan and the following metabolites in urine, related to the creatinine level, were measured: 5-hydroxyindoleacetic acid (5-HIAA), kynurenine (KYN), kynurenic acid (KYNA) and quinolinic acid (QA). (3) Results: In both groups of patients with IBS, changes in tryptophan metabolism were found as compared to the control group. We observed an increase in the activity of the serotonin pathway and a positive correlation between the 5-HIAA level and the GSRS score (p < 0.01) and HAM-A score (p < 0.001) in IBS-D patients. The IBS-C group was characterized by a higher concentration of kynurenines (KYN, QA) in urine. Moreover, the QA (p < 0.001) and KYNA (p < 0.05) levels were correlated with the HAM-D score among IBS-C patients. (4) Conclusions: Various changes in the tryptophan metabolism pathway can determine the differences in the clinical picture of irritable bowel syndrome. These results should be included in the nutritional and pharmacological treatment of this syndrome. Full article
(This article belongs to the Special Issue Nutrition, Gut Permeability, and Inflammation)
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17 pages, 22681 KiB  
Article
NAD Supplement Alleviates Intestinal Barrier Injury Induced by Ethanol Via Protecting Epithelial Mitochondrial Function
by Wenli Li, Yujia Zhou, Nengzhi Pang, Qianrong Hu, Qiuyan Li, Yan Sun, Yijie Ding, Yingying Gu, Ying Xiao, Mengqi Gao, Sixi Ma, Jie Pan, Evandro Fei Fang, Zhenfeng Zhang and Lili Yang
Nutrients 2023, 15(1), 174; https://doi.org/10.3390/nu15010174 - 30 Dec 2022
Cited by 11 | Viewed by 8329
Abstract
Background: The epithelial tight junction is an important intestinal barrier whose disruption can lead to the release of harmful intestinal substances into the circulation and cause damage to systemic injury. The maintenance of intestinal epithelial tight junctions is closely related to energy homeostasis [...] Read more.
Background: The epithelial tight junction is an important intestinal barrier whose disruption can lead to the release of harmful intestinal substances into the circulation and cause damage to systemic injury. The maintenance of intestinal epithelial tight junctions is closely related to energy homeostasis and mitochondrial function. Nicotinamide riboside (NR) is a NAD booster that can enhance mitochondrial biogenesis in liver. However, whether NR can prevent ethanol-induced intestinal barrier dysfunction and the underlying mechanisms remain unclear. Methods: We applied the mouse NIAAA model (chronic plus binge ethanol feeding) and Caco-2 cells to explore the effects of NR on ethanol-induced intestinal barrier dysfunction and the underlying mechanisms. NAD homeostasis and mitochondrial function were measured. In addition, knockdown of SirT1 in Caco-2 cells was further applied to explore the role of SirT1 in the protection of NR. Results: We found that ethanol increased intestinal permeability, increased the release of LPS into the circulation and destroyed the intestinal epithelial barrier structure in mice. NR supplementation attenuated intestinal barrier injury. Both in vivo and in vitro experiments showed that NR attenuated ethanol-induced decreased intestinal tight junction protein expressions and maintained NAD homeostasis. In addition, NR supplementation activated SirT1 activity and increased deacetylation of PGC-1α, and reversed ethanol-induced mitochondrial dysfunction and mitochondrial biogenesis. These effects were diminished with the knockdown of SirT1 in Caco-2 cells. Conclusion: Boosting NAD by NR alleviates ethanol-induced intestinal epithelial barrier damage via protecting mitochondrial function in a SirT1-dependent manner. Full article
(This article belongs to the Special Issue Nutrition, Gut Permeability, and Inflammation)
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17 pages, 2810 KiB  
Article
Polyphenol-Rich Liupao Tea Extract Prevents High-Fat Diet-Induced MAFLD by Modulating the Gut Microbiota
by Waijiao Tang, Mengfei Yuan, Zewen Li, Qi Lin, Yan Zhen, Zhuang Li, Hongwei Zhou and Fangbo Xia
Nutrients 2022, 14(22), 4930; https://doi.org/10.3390/nu14224930 - 21 Nov 2022
Cited by 3 | Viewed by 2516
Abstract
The modulation of gut microbiota dysbiosis might regulate the progression of metabolic-associated fatty liver disease (MAFLD). Here, we found that polyphenol-rich Liupao tea extract (PLE) prevents high-fat diet (HFD)-induced MAFLD in ApoE−/− male mice accompanied by protection of the intestinal barrier and [...] Read more.
The modulation of gut microbiota dysbiosis might regulate the progression of metabolic-associated fatty liver disease (MAFLD). Here, we found that polyphenol-rich Liupao tea extract (PLE) prevents high-fat diet (HFD)-induced MAFLD in ApoE−/− male mice accompanied by protection of the intestinal barrier and downregulation of lipopolysaccharide (LPS)-related Toll-like receptor 4 (TLR4)-myeloid differentiation primary response 88 (MyD88) signaling in the liver. Fecal microbiome transplantation (FMT) from PLE-and-HFD-treated mice delayed MAFLD development significantly compared with FMT from HFD-treated mice. In this case, 16S rRNA gene sequencing revealed that Rikenellaceae and Odoribacter were significantly enriched and that Helicobacter was significantly decreased in not only the HFD+PLE group but also the HFD+PLE-FMT group. Furthermore, the level of 3-sulfodeoxycholic acid was significantly decreased in the HFD+PLE-FMT group compared with the HFD-FMT group. In conclusion, our data demonstrate that PLE could modulate the MAFLD phenotype in mice and that this effect is partly mediated through modulation of the gut microbiota. Full article
(This article belongs to the Special Issue Nutrition, Gut Permeability, and Inflammation)
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