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Gut Microbiota and Metabolic Diseases 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Microbiology".

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 1489

Special Issue Editors


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Guest Editor
Department of Anaesthesia and Intensive Care, Chinese University of Hong Kong, Hong Kong 999077, China
Interests: cell proliferation; autophagy; colon cancer; gastric cancer
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Guest Editor
Lee Kong Chian School of Medicine, Nanyang Technological University of Singapore, Singapore 308232, Singapore
Interests: microbiome; nutrition; digestive diseases; metabolic syndrome; obesity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issue “Gut Microbiota and Metabolic Diseases”.

Metabolic diseases, including obesity, diabetes mellitus, dyslipidemia, and fatty liver disease, represent a global epidemic and markedly heighten the risks for potentially life-threatening complications, including cardiovascular diseases, cancer, and stroke. With the recent advancements in metagenomics, it has now been shown that these metabolic disorders are closely associated with dysbiotic gut microbiota. Functionally, metabolic-disease-associated gut microbes could contribute to disease development via disrupting the intestinal barrier function, releasing microbe-associated molecular patterns (MAMPs) and toxins, modulating bile acid metabolism, and producing immunologically and metabolically bioactive metabolites (e.g., branched-chain amino acids, trimethylamine). The gut microbiota is also directly involved in energy harvesting and controls satiety and food intake through the gut–brain axis. In this respect, modification of the gut microbiota has been proposed as a novel strategy to prevent or treat metabolic disorders.

This Special Issue is focused on the mechanistic aspect by which dysbiotic gut microbiota interact with the host to contribute to the pathogenesis of metabolic disorders. Potential topics also include the use of fecal microbiota transplantation and prebiotics/probiotics/postbiotics as novel therapeutics for ameliorating metabolic functions.

Dr. William K.K. Wu
Dr. Sunny H. Wong
Guest Editors

Manuscript Submission Information

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Keywords

  • metabolic syndromes
  • obesity
  • diabetes mellitus
  • microbiome
  • dyslipidemia
  • adiposity
  • insulin resistance
  • fatty liver disease

Published Papers (1 paper)

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Research

17 pages, 2342 KiB  
Article
Modulation of the Gut Microbiota by the Plantaricin-Producing Lactiplantibacillus plantarum D13, Analysed in the DSS-Induced Colitis Mouse Model
by Katarina Butorac, Jasna Novak, Martina Banić, Andreja Leboš Pavunc, Nina Čuljak, Nada Oršolić, Dyana Odeh, Jana Perica, Jagoda Šušković and Blaženka Kos
Int. J. Mol. Sci. 2023, 24(20), 15322; https://doi.org/10.3390/ijms242015322 - 18 Oct 2023
Cited by 1 | Viewed by 1161
Abstract
Lactiplantibacillus plantarum D13 shows antistaphylococcal and antilisterial activity, probably due to the synthesis of a presumptive bacteriocin with antibiofilm capacity released in the cell-free supernatant (CFS), whose inhibitory effect is enhanced by cocultivation with susceptible strains. An in silico analysis of the genome [...] Read more.
Lactiplantibacillus plantarum D13 shows antistaphylococcal and antilisterial activity, probably due to the synthesis of a presumptive bacteriocin with antibiofilm capacity released in the cell-free supernatant (CFS), whose inhibitory effect is enhanced by cocultivation with susceptible strains. An in silico analysis of the genome of strain D13 confirmed the pln gene cluster. Genes associated with plantaricin biosynthesis, structure, transport, antimicrobial activity, and immunity of strain D13 were identified. Furthermore, the predicted homology-based 3D structures of the cyclic conformation of PlnE, PlnF, PlnJ, and PlnK revealed that PlnE and PlnK contain two helices, while PlnF and PlnJ contain one and two helices, respectively. The potential of the strain to modulate the intestinal microbiota in healthy or dextran sulphate sodium (DSS)-induced colitis mouse models was also investigated. Strain D13 decreased the disease activity index (DAI) and altered the gut microbiota of mice with DSS-induced colitis by increasing the ratio of beneficial microbial species (Allobaculum, Barnesiella) and decreasing those associated with inflammatory bowel disease (Candidatus Saccharimonas). This suggests that strain D13 helps to restore the gut microbiota after DSS-induced colitis, indicating its potential for further investigation as a probiotic strain for the prevention and treatment of colitis. Full article
(This article belongs to the Special Issue Gut Microbiota and Metabolic Diseases 2.0)
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