Cited by 306Gut microbiota and healthAdipokines, Inflammation, and Metabolic DiseasesGastrointestinal motility and disorders

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Gut Microbiota, Intestinal Permeability, Obesity‐Induced Inflammation, and Liver Injury

Frazier, Thomas H., DiBaise, John K., McClain, Craig J.·2011·Journal of Parenteral and Enteral Nutrition

DOI 10.1177/0148607111413772

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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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“The use of this “humanized” mouse model may be very useful in future investigations on the role of diet and other interventions on the gut microbiota and its function.(33) Several other investigators have now confirmed changes in the microbiota composition and the development of an inflammatory response in mice ingest…”
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Authors: Frazier, T. H., DiBaise, J. K., & McClain, C. J.
Affiliations: University of Louisville (US)
Mayo Clinic (US)
Corresponding author: Frazier, Thomas H.
ORCID: DiBaise, John K.
McClain, Craig J.
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
DOI: 10.1177/0148607111413772
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: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
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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Gut Microbiota, Intestinal Permeability, Obesity‐Induced Inflammation, and Liver Injury

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