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Peer-reviewedCC BYNutrients

Gut Microbiome Dysbiosis in Metabolic Syndrome: Current Evidence and Emerging Perspectives

  • Fatma Shehata1
  • Karen M. Dwyer2
  • Sean L. McGee1
  • Leni R. Rivera1
  1. 1School of Medicine, Institute for Mental and Physical Health and Clinical Translation, Deakin University, Geelong, VIC 3220, Australia
  2. 2The Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC 3050, Australia
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Abstract

The gut microbiota plays a crucial role in human metabolism, and disruptions to its composition, particularly reductions in bacterial diversity, have been increasingly associated with the development of metabolic syndrome (MetS). MetS encompasses a constellation of interrelated metabolic risk factors, including central obesity, insulin resistance, dyslipidemia, and hypertension, which collectively elevate the risk of cardiovascular and cerebrovascular disease. A comprehensive understanding of the mechanisms underlying MetS is therefore critical for the development of effective preventive and therapeutic strategies. Complex interactions between the gut microbiota and host metabolic pathways are mediated by multiple factors, including microbial metabolites, inflammatory signaling, and host immune responses. This narrative review characterizes the clinical manifestations of MetS and alterations in gut microbiota composition, characterized by an overrepresentation of potentially pathogenic taxa and a concomitant decline in beneficial microbial species. In addition, we discuss current and emerging approaches to microbiota modulation, including prebiotics, probiotics, synbiotics, postbiotics, and fecal microbiota transplantation, and evaluate their potential roles in the prevention and management of MetS. We identify critical evidence gaps and propose research priorities for evidence-based clinical strategies for MetS management and prevention.

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Cite

BibTeXRIS
BibTeX
@article{shehata2026microbiome,
  title = {{Gut Microbiome Dysbiosis in Metabolic Syndrome: Current Evidence and Emerging Perspectives}},
  author = {Fatma Shehata and Karen M. Dwyer and Sean L. McGee and Leni R. Rivera},
  journal = {Nutrients},
  year = {2026},
  month = may,
  doi = {10.3390/nu18101540},
  url = {https://doi.org/10.3390/nu18101540},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Gut Microbiome Dysbiosis in Metabolic Syndrome: Current Evidence and Emerging Perspectives
AU  - Fatma Shehata
AU  - Karen M. Dwyer
AU  - Sean L. McGee
AU  - Leni R. Rivera
PY  - 2026
DA  - 2026/05/13
JO  - Nutrients
DO  - 10.3390/nu18101540
UR  - https://doi.org/10.3390/nu18101540
AB  - The gut microbiota plays a crucial role in human metabolism, and disruptions to its composition, particularly reductions in bacterial diversity, have been increasingly associated with the development of metabolic syndrome (MetS). MetS encompasses a constellation of interrelated metabolic risk factors, including central obesity, insulin resistance, dyslipidemia, and hypertension, which collectively elevate the risk of cardiovascular and cerebrovascular disease. A comprehensive understanding of the mechanisms underlying MetS is therefore critical for the development of effective preventive and therapeutic strategies. Complex interactions between the gut microbiota and host metabolic pathways are mediated by multiple factors, including microbial metabolites, inflammatory signaling, and host immune responses. This narrative review characterizes the clinical manifestations of MetS and alterations in gut microbiota composition, characterized by an overrepresentation of potentially pathogenic taxa and a concomitant decline in beneficial microbial species. In addition, we discuss current and emerging approaches to microbiota modulation, including prebiotics, probiotics, synbiotics, postbiotics, and fecal microbiota transplantation, and evaluate their potential roles in the prevention and management of MetS. We identify critical evidence gaps and propose research priorities for evidence-based clinical strategies for MetS management and prevention.
SN  - 2072-6643
ER  -