Diet, Gut Microbiota, and Gastrointestinal Disease

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

Deadline for manuscript submissions: 5 November 2024 | Viewed by 469

Special Issue Editor


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Guest Editor

Special Issue Information

Dear Colleagues,

Gastrointestinal diseases are a significant cause of morbidity and mortality worldwide. The recent advent of metagenomic techniques has highlighted the important role of the gut microbiota in human pathology.

The gut provides a vast interface area for the interaction between the host and the intestinal microbiota. At this level, the intricate crosstalk involves bacteria, surface cells, immune cells, endothelial cells, and nervous terminals. Moreover, there are several possible mediators involved in these interactions, such as microbial products, cytokines, and signalling factors, which make the scenario even more complex.

In this intricate conundrum, recent evidence has highlighted that some mechanisms of carcinogenesis may be strictly linked to dysbiosis and the detrimental effects of a derangement in the gut microbiota metabolism. Diet is a crucial modulator of the gut microbiota, and thus, it can be both detrimental, increasing the risk of gastrointestinal diseases via a more inflammatory and unhealthy gut microbiota, as well as helpful in restoring a balance in the gut microenvironment, resulting in a protective effect on disease development.

The Special Issue “Diet, Gut Microbiota, and Gastrointestinal Disease” aims to provide a platform for researchers with a keen interest in the study of this dynamic topic, specifically the interplay between diet/nutritional supplements, gut microbiota, and gastrointestinal diseases including cancer. Original articles and reviews focusing on this topic are welcome.

Dr. Francesca Romana Ponziani
Guest Editor

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Keywords

  • gut microbiota
  • diet
  • dietary supplements
  • inflammatory bowel diseases
  • coeliac disease
  • Helicobacter pylori
  • autoimmune gastritis
  • eosinophilic esophagitis
  • Crohn disease
  • ulcerative colitis
  • diverticular disease
  • irritable bowel syndrome
  • autoimmune hepatitis
  • viral hepatitis
  • metabolic dysfunction-associated steatotic liver disease
  • liver cancer
  • biliary tract cancers
  • pancreatic cancer
  • gastric cancer
  • esophageal cancer
  • colon cancer
  • host-microbiota interaction
  • inflammation
  • immunomodulation
  • metabolomics
  • personalized medicine

Published Papers (1 paper)

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Research

17 pages, 3302 KiB  
Article
Prebiotic Treatment in Patients with Nonalcoholic Fatty Liver Disease (NAFLD)—A Randomized Pilot Trial
by Naama Reshef, Uri Gophna, Leah Reshef, Fred Konikoff, Gila Gabay, Taiba Zornitzki, Hilla Knobler and Yaakov Maor
Nutrients 2024, 16(11), 1571; https://doi.org/10.3390/nu16111571 - 22 May 2024
Viewed by 356
Abstract
Several studies show that gut microbiotas in patients with nonalcoholic fatty liver disease (NAFLD) differ from those in a healthy population, suggesting that this alteration plays a role in NAFLD pathogenesis. We investigated whether prebiotic administration affects liver fat content and/or liver-related and [...] Read more.
Several studies show that gut microbiotas in patients with nonalcoholic fatty liver disease (NAFLD) differ from those in a healthy population, suggesting that this alteration plays a role in NAFLD pathogenesis. We investigated whether prebiotic administration affects liver fat content and/or liver-related and metabolic parameters. Patients with NAFLD and metabolic syndrome (age: 50 ± 11; 79% men) were randomized to receive either 16 g/day of prebiotic (ITFs—inulin-type fructans) (n = 8) or placebo (maltodextrin) (n = 11) for 12 weeks. Patients were instructed to maintain a stable weight throughout the study. Liver fat content (measured by H1MRS), fecal microbiota, and metabolic, inflammatory, and liver parameters were determined before and after intervention. Fecal samples from patients who received the prebiotic had an increased content of Bifidobacterium (p = 0.025), which was not observed with the placebo. However, the baseline and end-of-study liver fat contents did not change significantly in the prebiotic and placebo groups, neither did the liver function tests’ metabolic and inflammatory mediators, including fibroblast growth factor-19 and lipopolysaccharide-binding protein. Body weight remained stable in both groups. These findings suggest that prebiotic treatment without weight reduction is insufficient to improve NAFLD. Full article
(This article belongs to the Special Issue Diet, Gut Microbiota, and Gastrointestinal Disease)
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