Chronic sleep disruption alters gut microbiota, induces systemic and adipose tissue inflammation and insulin resistance in mice
Open accessAbstract
Chronic sleep fragmentation (SF) commonly occurs in human populations, and although it does not involve circadian shifts or sleep deprivation, it markedly alters feeding behaviors ultimately promoting obesity and insulin resistance. These symptoms are known to be related to the host gut microbiota. Mice were exposed to SF for 4 weeks and then allowed to recover for 2 weeks. Taxonomic profiles of fecal microbiota were obtained prospectively, and conventionalization experiments were performed in germ-free mice. Adipose tissue insulin sensitivity and inflammation, as well as circulating measures of inflammation, were assayed. Effect of fecal water on colonic epithelial permeability was also examined. Chronic SF-induced increased food intake and reversible gut microbiota changes characterized by the preferential growth of highly fermentative members of Lachnospiraceae and Ruminococcaceae and a decrease of Lactobacillaceae families. These lead to systemic and visceral white adipose tissue inflammation in addition to altered insulin sensitivity in mice, most likely via enhanced colonic epithelium barrier disruption. Conventionalization of germ-free mice with SF-derived microbiota confirmed these findings. Thus, SF-induced metabolic alterations may be mediated, in part, by concurrent changes in gut microbiota, thereby opening the way for gut microbiome-targeted therapeutics aimed at reducing the major end-organ morbidities of chronic SF.
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Increased abundance of Firmicutes and reduced abundance of Bacteroidetes in the gut microbiota have been observed in mice subjected to sleep fragmentation for 4 weeks.
“increased abundance of Firmicutes and reduced abundance of Bacteroidetes in the gut microbiota have been observed in mice subjected to sleep fragmentation for 4 weeks [48]”
From Gut microbiota and glucometabolic alterations in response to recurrent partial sleep deprivation in normal-weight young individuals (2016) · cites this paper as [48]
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- Authors
- Poroyko, V. A., Carreras, A., Khalyfa, A., Khalyfa, A. A., Leone, V., Peris, E., Almendros, I., Gileles-Hillel, A., Qiao, Z., Hubert, N., Farré, R., Chang, E. B., & Gozal, D.
- Affiliations
- City Of Hope National Medical Center (US)
- University of Chicago (US)
- Corresponding author
- Gozal, David
- ORCID
- Venue
- Scientific Reports
- Published
- 2016-10-14
- Volume
- 6
- Issue
- 1
- Pages
- 35405-35405
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC5064361
- OpenAlex
- W2531542945
- Cited by
- 480
- References
- 60
- Citations by year
- 2026: 38 · 2025: 63 · 2024: 72 · 2023: 56 · 2022: 53 · 2021: 61 · 2020: 53 · 2019: 29 · 2018: 35 · 2017: 18 · 2016: 2
- FWCI
- 14.47
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Dipòsit Digital de la Universitat de Barcelona (Universitat de Barcelona) (submittedVersion, cc-by)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK042086)
- 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 › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Keywords
- gut microbiota, insulin resistance, adipose tissue inflammation, visceral obesity, Lachnospiraceae, Ruminococcaceae, Lactobacillaceae, germ-free mice, conventionalization, dietary intake, gut barrier disruption
- MeSH terms
- Gastrointestinal Microbiome, Adipose Tissue, Animals, Insulin, Insulin Resistance, Interleukins, Lactobacillaceae, Male, Mice, Inbred C57BL, Sleep Deprivation, Leptin, Mice
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