Special Issue "Dietary Compounds Impact on Human Gut Microbiome and Gut Health"

A special issue of Nutrients (ISSN 2072-6643).

Deadline for manuscript submissions: closed (15 October 2019).

Special Issue Editor

Dr. Franck Gael Carbonero
E-Mail Website
Guest Editor
Department of Nutrition and Exercise Physiology, Elson Floyd School of Medicine, Washington State University-Spokane, 412 East Spokane Falls Boulevard, Spokane, 99202 WA, USA
Interests: microbiome; gut bacteria; nutrition, microbial ecology; polyphenols; berries; metabolomics

Special Issue Information

Dear Colleagues,

While it is somewhat controversial that “you are what you eat”, there is increasing evidence that “your gut microbiome is what you eat”. Indeed, countless studies have shown that short- or long-term dietary habits result in distinct gut microbiome signatures. In the context of personalized medicine and nutrition, there is a crucial need for predictive models of the impact of specific dietary compounds on gut microbiome and gut health. The purpose of this Special Issue is therefore to provide a platform for researchers to report novel findings on the interplay between dietary bioactive compounds (defined as those available for microbial degradation and other metabolic pathways), the gut microbiome (and its associated metabolome), and gut health (especially inflammation and immunity markers).

Dr. Franck Gael Carbonero
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 papers will be 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 monthly 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 2000 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

  • Gut Microbiome/Microbiota
  • Dietary bioactives
  • Human Nutrition
  • Gut Health
  • Metabolome
  • Inflammation

Published Papers (6 papers)

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Research

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Open AccessArticle
Potato-Resistant Starch Supplementation Improves Microbiota Dysbiosis, Inflammation, and Gut–Brain Signaling in High Fat-Fed Rats
Nutrients 2019, 11(11), 2710; https://doi.org/10.3390/nu11112710 - 08 Nov 2019
Abstract
(1) High-fat (HF) diet leads to gut microbiota dysbiosis which is associated with systemic inflammation. Bacterial-driven inflammation is sufficient to alter vagally mediated satiety and induce hyperphagia. Promoting bacterial fermentation improves gastrointestinal (GI) epithelial barrier function and reduces inflammation. Resistant starch escape digestion [...] Read more.
(1) High-fat (HF) diet leads to gut microbiota dysbiosis which is associated with systemic inflammation. Bacterial-driven inflammation is sufficient to alter vagally mediated satiety and induce hyperphagia. Promoting bacterial fermentation improves gastrointestinal (GI) epithelial barrier function and reduces inflammation. Resistant starch escape digestion and can be fermented by bacteria in the distal gut. Therefore, we hypothesized that potato RS supplementation in HF-fed rats would lead to compositional changes in microbiota composition associated with improved inflammatory status and vagal signaling. (2) Male Wistar rats (n = 8/group) were fed a low-fat chow (LF, 13% fat), HF (45% fat), or an isocaloric HF supplemented with 12% potato RS (HFRS) diet. (3) The HFRS-fed rats consumed significantly less energy than HF animals throughout the experiment. Systemic inflammation and glucose homeostasis were improved in the HFRS compared to HF rats. Cholecystokinin-induced satiety was abolished in HF-fed rats and restored in HFRS rats. HF feeding led to a significant decrease in positive c fiber staining in the brainstem which was averted by RS supplementation. (4) The RS supplementation prevented dysbiosis and systemic inflammation. Additionally, microbiota manipulation via dietary potato RS prevented HF-diet-induced reorganization of vagal afferent fibers, loss in CCK-induced satiety, and hyperphagia. Full article
(This article belongs to the Special Issue Dietary Compounds Impact on Human Gut Microbiome and Gut Health)
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Open AccessCommunication
Tea Compounds and the Gut Microbiome: Findings from Trials and Mechanistic Studies
Nutrients 2019, 11(10), 2364; https://doi.org/10.3390/nu11102364 - 03 Oct 2019
Abstract
In recent years, the gut microbiome has become a focal point of interest with growing recognition that a well-balanced gut microbiota composition is highly relevant to an individual’s health status and well-being. Its profile can be modulated by a number of dietary factors, [...] Read more.
In recent years, the gut microbiome has become a focal point of interest with growing recognition that a well-balanced gut microbiota composition is highly relevant to an individual’s health status and well-being. Its profile can be modulated by a number of dietary factors, although few publications have focused on the effects of what we drink. The present review performed a systematic review of trials and mechanistic studies examining the effects of tea consumption, its associated compounds and their effects on the gut microbiome. Registered articles were searched up to 10th September 2019, in the PubMed and Cochrane library databases along with references of original articles. Human trials were graded using the Jadad scale to assess quality. Altogether 24 publications were included in the main review—six were human trials and 18 mechanistic studies. Of these, the largest body of evidence related to green tea with up to 1000 mL daily (4–5 cups) reported to increase proportions of Bifidobacterium. Mechanistic studies also show promise suggesting that black, oolong, Pu-erh and Fuzhuan teas (microbially fermented ‘dark tea’) can modulate microbial diversity and the ratio of Firmicutes to Bacteroidetes. These findings appear to support the hypothesis that tea ingestion could favourably regulate the profile of the gut microbiome and help to offset dysbiosis triggered by obesity or high-fat diets. Further well-designed human trials are now required to build on provisional findings. Full article
(This article belongs to the Special Issue Dietary Compounds Impact on Human Gut Microbiome and Gut Health)
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Open AccessArticle
Laminaria japonica Extract Enhances Intestinal Barrier Function by Altering Inflammatory Response and Tight Junction-Related Protein in Lipopolysaccharide-Stimulated Caco-2 Cells
Nutrients 2019, 11(5), 1001; https://doi.org/10.3390/nu11051001 - 01 May 2019
Cited by 2
Abstract
In the normal physiological state, intestinal epithelial cells act as a defensive frontline of host mucosal immunity to tolerate constant exposure to external stimuli. In this study, we investigated the potential anti-inflammatory and gut permeability protective effects of Laminaria japonica (LJ) water extract [...] Read more.
In the normal physiological state, intestinal epithelial cells act as a defensive frontline of host mucosal immunity to tolerate constant exposure to external stimuli. In this study, we investigated the potential anti-inflammatory and gut permeability protective effects of Laminaria japonica (LJ) water extract (LJE) and three types of fermented Laminaria japonica water extracts (LJE-F1, LJE-F2, and LJE-F3) in lipopolysaccharide (LPS)-stimulated Caco-2, human intestinal epithelial cells. All four extracts significantly decreased the production of nitric oxide and interleukin-6 induced by LPS stimulus. In addition, LJE and the three types of LJE-Fs also inhibited LPS-induced loss of monolayer permeability, as assessed by changes in transepithelial electrical resistance. All four LJ extracts significantly prevented the inhibition of the protein levels of occludin, whereas LJE, LJE-F1, and LJE-F3 significantly attenuated the reduction in phosphorylation of adenosine monophosphate-activated protein kinase compared with the LPS-treated group in Caco-2 cells. In conclusion, LJE and its fermented water extracts appear to have potential gut health-promoting effects by reducing inflammation and partially regulating the tight junction-related proteins in human intestinal epithelial cells. Thus, additional studies are warranted to evaluate Laminaria japonica as a therapeutic agent for inflammatory bowel diseases. Full article
(This article belongs to the Special Issue Dietary Compounds Impact on Human Gut Microbiome and Gut Health)
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Open AccessArticle
Transcriptional Regulation of the Equol Biosynthesis Gene Cluster in Adlercreutzia equolifaciens DSM19450T
Nutrients 2019, 11(5), 993; https://doi.org/10.3390/nu11050993 - 30 Apr 2019
Cited by 1
Abstract
Given the emerging evidence of equol’s benefit to human health, understanding its synthesis and regulation in equol-producing bacteria is of paramount importance. Adlercreutzia equolifaciens DSM19450T is a human intestinal bacterium—for which the whole genome sequence is publicly available—that produces equol from the [...] Read more.
Given the emerging evidence of equol’s benefit to human health, understanding its synthesis and regulation in equol-producing bacteria is of paramount importance. Adlercreutzia equolifaciens DSM19450T is a human intestinal bacterium—for which the whole genome sequence is publicly available—that produces equol from the daidzein isoflavone. In the present work, daidzein (between 50 to 200 μM) was completely metabolized by cultures of A. equolifaciens DSM19450T after 10 h of incubation. However, only about one third of the added isoflavone was transformed into dihydrodaidzein and then into equol. Transcriptional analysis of the ORFs and intergenic regions of the bacterium’s equol gene cluster was therefore undertaken using RT-PCR and RT-qPCR techniques with the aim of identifying the genetic elements of equol biosynthesis and its regulation mechanisms. Compared to controls cultured without daidzein, the expression of all 13 contiguous genes in the equol cluster was enhanced in the presence of the isoflavone. Depending on the gene and the amount of daidzein in the medium, overexpression varied from 0.5- to about 4-log10 units. Four expression patterns of transcription were identified involving genes within the cluster. The genes dzr, ddr and tdr, which code for daidzein reductase, dihydrodaidzein reductase and tetrahydrodaidzein reductase respectively, and which have been shown involved in equol biosynthesis, were among the most strongly expressed genes in the cluster. These expression patterns correlated with the location of four putative ρ-independent terminator sequences in the cluster. All the intergenic regions were amplified by RT-PCR, indicating the operon to be transcribed as a single RNA molecule. These findings provide new knowledge on the metabolic transformation of daidzein into equol by A. equolifaciens DSM19450T, which might help in efforts to increase the endogenous formation of this compound and/or its biotechnological production. Full article
(This article belongs to the Special Issue Dietary Compounds Impact on Human Gut Microbiome and Gut Health)
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Review

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Open AccessReview
Impact of Food Additives on Gut Homeostasis
Nutrients 2019, 11(10), 2334; https://doi.org/10.3390/nu11102334 - 01 Oct 2019
Abstract
In physiological conditions, the gut is heavily infiltrated with various subsets of inflammatory cells, whose activity is tightly controlled by counter-regulatory mechanisms. Defects in such mechanisms can favour the development of chronic intestinal disorders, such as Crohn’s disease (CD) and ulcerative colitis (UC), [...] Read more.
In physiological conditions, the gut is heavily infiltrated with various subsets of inflammatory cells, whose activity is tightly controlled by counter-regulatory mechanisms. Defects in such mechanisms can favour the development of chronic intestinal disorders, such as Crohn’s disease (CD) and ulcerative colitis (UC), the principal forms of inflammatory bowel diseases (IBD) in humans, as well as systemic disorders. Over the last years, the frequency of intestinal and systemic immune-inflammatory disorders has increased in previously low incidence areas, likely due to the Westernization of lifestyles, including dietary habits. The Western diet is characterized by high consumption of proteins, saturated fats and sweets, as well as by a broad use of food additives (e.g., emulsifiers, bulking agents), which are used to preserve and enhance food quality. Accumulating evidence suggests that food additives can perturb gut homeostasis, thereby contributing to promote tissue-damaging inflammatory responses. For instance, mice given the emulsifiers carboxymethylcellulose and polysorbate 80 develop dysbiosis with overgrowth of mucus-degrading bacteria. Such an effect triggers colitis in animals deficient in either interleukin-10, a cytokine exerting anti-inflammatory and regulatory functions, or Toll-like receptor 5, a receptor recognizing the bacterial flagellin. Similarly, the polysaccharide maltodextrin induces endoplasmic reticulum stress in intestinal goblet cells, thereby impairing mucus release and increasing host susceptibility to colitis. In this review, we report and discuss the current knowledge about the impact of food additives on gut homeostasis and their potential contribution to the development of inflammatory disorders. Full article
(This article belongs to the Special Issue Dietary Compounds Impact on Human Gut Microbiome and Gut Health)
Open AccessReview
Regulation of Gut Microbiota and Metabolic Endotoxemia with Dietary Factors
Nutrients 2019, 11(10), 2277; https://doi.org/10.3390/nu11102277 - 23 Sep 2019
Abstract
Metabolic endotoxemia is a condition in which blood lipopolysaccharide (LPS) levels are elevated, regardless of the presence of obvious infection. It has been suggested to lead to chronic inflammation-related diseases such as obesity, type 2 diabetes mellitus, non-alcoholic fatty liver disease (NAFLD), pancreatitis, [...] Read more.
Metabolic endotoxemia is a condition in which blood lipopolysaccharide (LPS) levels are elevated, regardless of the presence of obvious infection. It has been suggested to lead to chronic inflammation-related diseases such as obesity, type 2 diabetes mellitus, non-alcoholic fatty liver disease (NAFLD), pancreatitis, amyotrophic lateral sclerosis, and Alzheimer’s disease. In addition, it has attracted attention as a target for the prevention and treatment of these chronic diseases. As metabolic endotoxemia was first reported in mice that were fed a high-fat diet, research regarding its relationship with diets has been actively conducted in humans and animals. In this review, we summarize the relationship between fat intake and induction of metabolic endotoxemia, focusing on gut dysbiosis and the influx, kinetics, and metabolism of LPS. We also summarize the recent findings about dietary factors that attenuate metabolic endotoxemia, focusing on the regulation of gut microbiota. We hope that in the future, control of metabolic endotoxemia using dietary factors will help maintain human health. Full article
(This article belongs to the Special Issue Dietary Compounds Impact on Human Gut Microbiome and Gut Health)
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