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Persistent alterations in glucose metabolism, gut microbiome, and adipose tissue transcriptome after two-week sleep recovery in chronically sleep-fragmented female mice

ABSTRACT: Introduction: Chronic sleep fragmentation (SF) is prevalent in contemporary human society, highlighting detrimental effects on glucose metabolism and adipose tissue morphology, which is closely linked to gut microbiota composition. However, it remains unclear whether sleep recovery (SR) after prolonged SF can ameliorate glucose metabolism, influence the transcriptome of inguinal white adipose tissue (iWAT), and whether these effects align with alterations in the gut microbiota. Methods: Mice were subjected to 8 weeks of SF and subsequently allowed 2 weeks of SR. We assessed glucose tolerance through intraperitoneal glucose tolerance tests (ipGTT), analyzed gut microbiota via 16s rDNA amplicon sequencing, and examined transcriptomic alterations in iWAT using RNA sequencing. Results: Despite the two-week SR following chronic SF, significant glucose intolerance persisted, accompanied by subtle shifts in the gut microbiota and alterations in gene expression within iWAT. The top hub genes Ncapg, Cenpe, and Tik were identified from the protein-protein interaction network. Conclusion: Even followed by a brief period of SR, prolonged SF still led to ongoing glucose intolerance and alterations in the adipose tissue transcriptome in mice. These changes were intertwined with modifications in the gut microbiome. The shifts in gut microbiota may play a pivotal role in understanding the sustained negative effects of SF.

ORGANISM(S): Mus musculus

PROVIDER: GSE248189 | GEO | 2024/06/30

REPOSITORIES: GEO

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Project description:Background & Aims: Non-alcoholic fatty liver disease (NALFLD)-associated changes in gut microbiota are important drivers of disease progression toward fibrosis. Therefore, reversing microbiota alterations could ameliorate NAFLD progression. Oat beta-glucan, a non-digestible polysaccharides, has shown promising therapeutic effects on hyperlipidemia associated with NAFLD, but its impact on gut microbiota and most importantly NAFLD fibrosis remains unknown. Methods: We performed detailed metabolic phenotyping including body composition, glucose tolerance, and lipid metabolism as well as comprehensive characterization of the gut-liver axis in a western-style diet (WSD)-induced model of NAFLD and assessed the effect of a beta-glucan intervention on early and advanced liver disease. Gut microbiota was modulated using broad-spectrum antibiotic (Abx) treatment. Results: Oat beta-glucan supplementation did not affect WSD-induced body weight gain, glucose intolerance, and the metabolic phenotype remained largely unaffected. Interestingly, oat beta-glucan dampened NAFLD inflammation, associated with significantly reduced monocyte-derived macrophages (MoMFs) infiltration, fibroinflammatory gene expression, and strongly reduced fibrosis development. Mechanistically, this protective effect was not mediated by changes in bile acid composition or signaling, but was dependent on gut microbiota and was lost upon Abx treatment. Specifically, oat beta-glucan partially reversed unfavorable changes in gut microbiota, resulting in an expansion of protective taxa, including Ruminococcus, and Lactobacillus followed by reduced translocation of TLR ligands. Conclusions: Our findings identify oat beta-glucan as a highly efficacious food supplement that dampens inflammation and fibrosis development in diet-induced NAFLD. These results, along with its favorable dietary profile, suggest that it may be a cost-effective and well-tolerated approach to preventing NAFLD progression and should be assessed in clinical studies.

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Persistent alterations in glucose metabolism, gut microbiome, and adipose tissue transcriptome after two-week sleep recovery in chronically sleep-fragmented female mice

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