Increased oral detection, but decreased intestinal signaling for fats in mice lacking gut microbiota
Open accessAbstract
Germ-free (GF) mice lacking intestinal microbiota are significantly leaner than normal (NORM) control mice despite consuming more calories. The contribution of microbiota on the recognition and intake of fats is not known. Thus, we investigated the preference for, and acceptance of, fat emulsions in GF and NORM mice, and associated changes in lingual and intestinal fatty acid receptors, intestinal peptide content, and plasma levels of gut peptides. GF and NORM C57Bl/6J mice were given 48-h two-bottle access to water and increasing concentrations of intralipid emulsions. Gene expression of the lingual fatty acid translocase CD36 and protein expression of intestinal satiety peptides and fatty-acid receptors from isolated intestinal epithelial cells were determined. Differences in intestinal enteroendocrine cells along the length of the GI tract were quantified. Circulating plasma satiety peptides reflecting adiposity and biochemical parameters of fat metabolism were also examined. GF mice had an increased preference and intake of intralipid relative to NORM mice. This was associated with increased lingual CD36 (P<0.05) and decreased intestinal expression of fatty acid receptors GPR40 (P<0.0001), GPR41 (P<0.0001), GPR43 (P<0.05), and GPR120 (P<0.0001) and satiety peptides CCK (P<0.0001), PYY (P<0.001), and GLP-1 (P<0.001). GF mice had fewer enteroendocrine cells in the ileum (P<0.05), and more in the colon (P<0.05), relative to NORM controls. Finally, GF mice had lower levels of circulating leptin and ghrelin (P<0.001), and altered plasma lipid metabolic markers indicative of energy deficits. Increased preference and caloric intake from fats in GF mice are associated with increased oral receptors for fats coupled with broad and marked decreases in expression of intestinal satiety peptides and fatty-acid receptors.
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Germ-free mice have lower levels of plasma ghrelin under basal conditions than conventional mice.
“Indeed, germ-free mice have lower levels of plasma ghrelin under basal conditions than conventional mice [128,129].”
From Anxiety, depression, and the microbiome: A role for gut peptides (2018) · cites this paper as [128]
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- Authors
- Duca, F. A., Swartz, T. D., Sakar, Y., & Covasa, M.
- Affiliations
- Microbiologie de l’alimentation au service de la santé (FR)
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-06-29
- Volume
- 7
- Issue
- 6
- Pages
- e39748
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3387243
- OpenAlex
- W2061559910
- Cited by
- 181
- References
- 40
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 17 · 2023: 12 · 2022: 15 · 2021: 14 · 2020: 24 · 2019: 21 · 2018: 16 · 2017: 14 · 2016: 9 · 2015: 8 · 2014: 10 · 2013: 7
- FWCI
- 3.22
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Institut National de la Recherche Agronomique
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Keywords
- gut microbiota, germ-free mice, dietary fat intake, fat preference, fatty acid receptor, CD36, GPR40, GPR41, GPR43, GPR120, satiety peptides, cholecystokinin, peptide YY, glucagon-like peptide-1, enteroendocrine cells, leptin, ghrelin, energy homeostasis, lipid emulsions
- MeSH terms
- Animals, Blood Glucose, Body Weight, Energy Intake, Cell Count, Emulsions, Gastrointestinal Hormones, Gene Expression Regulation, Germ-Free Life, Intestinal Mucosa, Intestines, Lipids, Male, Mice, Inbred C57BL, Mouth, Oils, Peptides, Signal Transduction, CD36 Antigens, Enteroendocrine Cells, Lipid Metabolism, Mice, Metagenome
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