The role of the gut microbiota in energy metabolism and metabolic disease
Abstract
Obesity is now classically characterized by a cluster of several metabolic disorders, and by a low grade inflammation. The evidence that the gut microbiota composition can be different between healthy and or obese and type 2 diabetic patients has led to the study of this environmental factor as a key link between the pathophysiology of metabolic diseases and the gut microbiota. Several mechanisms are proposed linking events occurring in the colon and the regulation of energy metabolism, such as i.e. the energy harvest from the diet, the synthesis of gut peptides involved in energy homeostasis (GLP-1, PYY...), and the regulation of fat storage. Moreover, the development of obesity and metabolic disorders following a high-fat diet may be associated to the innate immune system. Indeed, high-fat diet feeding triggers the development of obesity, inflammation, insulin resistance, type 2 diabetes and atherosclerosis by mechanisms dependent of the LPS and/or the fatty acids activation of the CD14/TLR4 receptor complex. Importantly, fat feeding is also associated with the development of metabolic endotoxemia in human subjects and participates in the low-grade inflammation, a mechanism associated with the development of atherogenic markers. Finally, data obtained in experimental models and human subjects are in favour of the fact that changing the gut microbiota (with prebiotics and/or probiotics) may participate in the control of the development of metabolic diseases associated with obesity. Thus, it would be useful to find specific strategies for modifying gut microbiota to impact on the occurrence of metabolic diseases.
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Short-chain fatty acids produced by the gut microbiota metabolism of resistant starch and oligosaccharides present in the Mediterranean diet can induce satiety by inhibiting gastric emptying through increased production of gut hormones such as GLP-1 and PYY.
“It has been hypothesized that the short-chain fatty acids produced by the gut microbiota metabolism of the great bulk of resistant starch and oligosaccharides present in the Mediterranean diet can induce satiety by inhibiting gastric emptying through the increased production of gut hormones, such as glucagon like peptide-1 (GLP-1) and peptide-YY (PYY) (67).”
From Health Benefits of the Mediterranean Diet: Metabolic and Molecular Mechanisms (2018) · cites this paper as [67]
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- Authors
- Cani, P., & Delzenne, N.
- Affiliations
- UCLouvain (BE)
- Corresponding author
- Delzenne, Nathalie
- Venue
- Current Pharmaceutical Design
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2009-05-01
- Volume
- 15
- Issue
- 13
- Pages
- 1546-1558
- ISSN
- 1381-6128 (ISSN-L)
- OpenAlex
- W1972686367
- Cited by
- 974
- References
- 110
- Citations by year
- 2026: 36 · 2025: 51 · 2024: 49 · 2023: 41 · 2022: 56 · 2021: 63 · 2020: 70 · 2019: 55 · 2018: 67 · 2017: 66 · 2016: 73 · 2015: 61 · 2014: 53 · 2013: 72 · 2012: 41
- FWCI
- 21.59
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Pharmaceutical Design (publishedVersion)
- PubMed (publishedVersion)
- Digital Access to Libraries (Université catholique de Louvain (UCL), l'Université de Namur (UNamur) and the Université Saint-Louis (USL-B)) (submittedVersion)
- Funders
- Université Catholique de Louvain
- Fonds Spéciaux de Recherche
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
- Keywords
- gut microbiota, energy metabolism, obesity, type 2 diabetes, metabolic disorders, low-grade inflammation, insulin resistance, atherosclerosis, high-fat diet, endotoxemia, lipopolysaccharide, gut peptides, glucagon-like peptide-1, peptide YY, fat deposition, prebiotics, probiotics, gut-brain axis
- MeSH terms
- Animals, Dietary Fats, Energy Metabolism, Humans, Immunity, Innate, Metabolic Diseases, Obesity, Probiotics, Gastrointestinal Tract
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