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Gut Microbiota, Intestinal Permeability, Obesity‐Induced Inflammation, and Liver Injury
Abstract
Obesity and its metabolic complications are major health problems in the United States and worldwide, and increasing evidence implicates the microbiota in these important health issues. Indeed, it appears that the microbiota function much like a metabolic “organ,” influencing nutrient acquisition, energy homeostasis, and, ultimately, the control of body weight. Moreover, alterations in gut microbiota, increased intestinal permeability, and metabolic endotoxemia likely play a role in the development of a chronic low‐grade inflammatory state in the host that contributes to the development of obesity and associated chronic metabolic diseases such as nonalcoholic fatty liver disease. Supporting these concepts are the observations that increased gut permeability, low‐grade endotoxemia, and fatty liver are observed in animal models of obesity caused by either high‐fat or high‐fructose feeding. Consistent with these observations, germ‐free mice are protected from obesity and many forms of liver injury. Last, many agents that affect gut flora/permeability, such as probiotics/prebiotics, also appear to affect obesity and certain forms of liver injury in animal model systems. Here the authors review the role of the gut microbiota and metabolic endotoxemia‐induced inflammation in the development of obesity and liver injury, with special reference to the intensive care unit setting.
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“dysbiosis in the gut has been shown to induce increased permeability of the intestine, leading to increased systemic levels of bacterial products causing low-grade chronic inflammation.”
From The Gut Microbiome Contributes to a Substantial Proportion of the Variation in Blood Lipids (2015) · cites this paper as [10]
In the citing paper
“In the gut, the GM and its metabolites have been shown to modulate gastrointestinal functions via their effects on intestinal permeability (32–35), mucosal immune function (36–38), intestinal motility and sensitivity (39, 40), and the enteric nervous system (ENS) (21, 24, 25, 41).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [34]
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Metadata
- Authors
- Frazier, T. H., DiBaise, J. K., & McClain, C. J.
- Affiliations
- University of Louisville (US)
- Mayo Clinic (US)
- Corresponding author
- Frazier, Thomas H.
- Venue
- Journal of Parenteral and Enteral Nutrition
- Publisher
- Wiley
- Published
- 2011-08
- Volume
- 35
- Issue
- 5S
- Pages
- 14S-20S
- ISSN
- 0148-6071 (ISSN-L)
- 1941-2444
- OpenAlex
- W2029789888
- Cited by
- 306
- References
- 58
- Citations by year
- 2026: 4 · 2025: 13 · 2024: 9 · 2023: 20 · 2022: 26 · 2021: 31 · 2020: 27 · 2019: 25 · 2018: 23 · 2017: 21 · 2016: 18 · 2015: 25 · 2014: 27 · 2013: 23 · 2012: 13
- FWCI
- 1.86
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Journal of Parenteral and Enteral Nutrition (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Keywords
- gut microbiota, intestinal permeability, obesity, low-grade inflammation, endotoxemia, non-alcoholic fatty liver disease, liver injury, germ-free mice, probiotics, prebiotics, high-fat feeding, energy homeostasis, intensive care unit
- MeSH terms
- Animals, Body Weight, Disease Models, Animal, Humans, Inflammation, Liver Diseases, Metabolic Diseases, Obesity, Guidelines as Topic, Endotoxemia, Probiotics, Gastrointestinal Tract, Mice, Metagenome, Prebiotics, Diet, High-Fat
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