Gut microbiota, enteroendocrine functions and metabolism
Abstract
The gut microbiota affects host metabolism through a number of physiological processes. Emerging evidence suggests that gut microbes interact with the host through several pathways involving enteroendocrine cells (e.g. L cells). The activation of specific G protein coupled receptors expressed on L cells (e.g. GPR41, GPR43, GPR119 and TGR5) triggers the secretion of glucagon-like peptides (GLP-1 and GLP-2) and PYY. These gut peptides are known to control energy homeostasis, glucose metabolism, gut barrier function and metabolic inflammation. Here, we explore how crosstalk between the ligands produced by the gut microbiota (short chain fatty acids, or SCFAs), or produced by the host but influenced by gut microbes (endocannabinoids and bile acids), impact host physiology.
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The microbiota regulates, via different mechanisms, some important physiological functions of the host, such as those related to energy expenditure, satiety and glucose homeostasis.
“The microbiota regulates, via different mechanisms, some important physiological functions of the host, such as those related to energy expenditure, satiety and glucose homeostasis [10,11] .”
From Intestinal microbiota in health and disease: Role of bifidobacteria in gut homeostasis (2014) · cites this paper as [10]
The GM can stimulate the release of peptides and hormones from enteroendocrine cells, which can have direct or indirect central effects.
“The GM can stimulate the release of peptides and hormones from enteroendocrine cells, which can have direct or indirect central effects (22, 39).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [39]
In the gut, the GM and its metabolites modulate gastrointestinal functions via effects on intestinal permeability, mucosal immune function, intestinal motility and sensitivity, and the ENS.
“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 [39]
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- Authors
- Cani, P. D., Everard, A., & Duparc, T.
- Affiliations
- Walloon Excellence in Lifesciences and Biotechnology (BE)
- Corresponding author
- Cani, Patrice D
- Venue
- Current Opinion in Pharmacology
- Publisher
- Elsevier BV
- Published
- 2013-12
- Volume
- 13
- Issue
- 6
- Pages
- 935-940
- ISSN
- 1471-4892 (ISSN-L)
- OpenAlex
- W2044719746
- Cited by
- 378
- References
- 61
- Citations by year
- 2026: 16 · 2025: 17 · 2024: 21 · 2023: 26 · 2022: 31 · 2021: 37 · 2020: 45 · 2019: 34 · 2018: 48 · 2017: 36 · 2016: 29 · 2015: 21 · 2014: 16 · 2013: 1
- FWCI
- 2.10
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Opinion in Pharmacology (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)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- gut microbiota, enteroendocrine cells, L cells, G protein-coupled receptors, GPR41, GPR43, GPR119, TGR5, glucagon-like peptide-1, glucagon-like peptide-2, peptide YY, short-chain fatty acids, endocannabinoids, bile acids, energy homeostasis, glucose metabolism, intestinal barrier, metabolic inflammation
- MeSH terms
- Animals, Gastrointestinal Hormones, Humans, Enteroendocrine Cells, Gastrointestinal Tract, Microbiota
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