Soybean oil-based HFD induces gut dysbiosis that leads to steatosis, hepatic inflammation and insulin resistance in mice.

gut dysbiosis inflammation insulin resistance steatosis sucrose free HFD

Journal

Frontiers in microbiology
ISSN: 1664-302X
Titre abrégé: Front Microbiol
Pays: Switzerland
ID NLM: 101548977

Informations de publication

Date de publication:
2024
Historique:
received: 26 03 2024
accepted: 09 07 2024
medline: 21 8 2024
pubmed: 21 8 2024
entrez: 21 8 2024
Statut: epublish

Résumé

High-fat diets (HFDs) shape the gut microbiome and promote obesity, inflammation, and liver steatosis. Fish and soybean are part of a healthy diet; however, the impact of these fats, in the absence of sucrose, on gut microbial dysbiosis and its association with liver steatosis remains unclear. Here, we investigated the effect of sucrose-free soybean oil-and fish oil-based high fat diets (HFDs) (SF-Soy-HFD and SF-Fish-HFD, respectively) on gut dysbiosis, obesity, steatosis, hepatic inflammation, and insulin resistance. C57BL/6 mice were fed these HFDs for 24 weeks. Both diets had comparable effects on liver and total body weights. But 16S-rRNA sequencing of the gut content revealed induction of gut dysbiosis at different taxonomic levels. The microbial communities were clearly separated, showing differential dysbiosis between the two HFDs. Compared with the SF-Fish-HFD control group, the SF-Soy-HFD group had an increased abundance of Bacteroidetes, Firmicutes, and Deferribacteres, but a lower abundance of Verrucomicrobia. The Clostridia/Bacteroidia (C/B) ratio was higher in the SF-Soy-HFD group (3.11) than in the SF-Fish-HFD group (2.5). Conversely, the Verrucomicrobiacae/S24_7 (also known as Muribaculaceae family) ratio was lower in the SF-Soy-HFD group (0.02) than that in the SF-Fish-HFD group (0.75). The SF-Soy-HFD group had a positive association with S24_7, Clostridiales, Allobaculum, Coriobacteriaceae, Adlercreutzia, Christensenellaceae, Lactococcus, and Oscillospira, but was related to a lower abundance of Akkermansia, which maintains gut barrier integrity. The gut microbiota in the SF-Soy-HFD group had predicted associations with host genes related to fatty liver and inflammatory pathways. Mice fed the SF-Soy-HFD developed liver steatosis and showed increased transcript levels of genes associated with

Identifiants

pubmed: 39165573
doi: 10.3389/fmicb.2024.1407258
pmc: PMC11334085
doi:

Types de publication

Journal Article

Langues

eng

Pagination

1407258

Informations de copyright

Copyright © 2024 Jacob, Sindhu, Hasan, Malik, Arefanian, Al-Rashed, Nizam, Kochumon, Thomas, Bahman, Shenouda, Wilson, Akther, Al-Roub, Abukhalaf, Albeloushi, Abu-Farha, Al Madhoun, Alzaid, Thanaraj, Koistinen, Tuomilehto, Al-Mulla and Ahmad.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.

Auteurs

Texy Jacob (T)

Dasman Diabetes Institute, Dasman, Kuwait.

Sardar Sindhu (S)

Dasman Diabetes Institute, Dasman, Kuwait.

Amal Hasan (A)

Dasman Diabetes Institute, Dasman, Kuwait.

Md Zubbair Malik (MZ)

Dasman Diabetes Institute, Dasman, Kuwait.

Hossein Arefanian (H)

Dasman Diabetes Institute, Dasman, Kuwait.

Fatema Al-Rashed (F)

Dasman Diabetes Institute, Dasman, Kuwait.

Rasheeba Nizam (R)

Dasman Diabetes Institute, Dasman, Kuwait.

Shihab Kochumon (S)

Dasman Diabetes Institute, Dasman, Kuwait.

Reeby Thomas (R)

Dasman Diabetes Institute, Dasman, Kuwait.

Fatemah Bahman (F)

Dasman Diabetes Institute, Dasman, Kuwait.

Steve Shenouda (S)

Dasman Diabetes Institute, Dasman, Kuwait.

Ajit Wilson (A)

Dasman Diabetes Institute, Dasman, Kuwait.

Nadeem Akther (N)

Dasman Diabetes Institute, Dasman, Kuwait.

Areej Al-Roub (A)

Dasman Diabetes Institute, Dasman, Kuwait.

Nermeen Abukhalaf (N)

Dasman Diabetes Institute, Dasman, Kuwait.

Shaima Albeloushi (S)

Dasman Diabetes Institute, Dasman, Kuwait.

Mohamed Abu-Farha (M)

Dasman Diabetes Institute, Dasman, Kuwait.

Ashraf Al Madhoun (A)

Dasman Diabetes Institute, Dasman, Kuwait.

Fawaz Alzaid (F)

Dasman Diabetes Institute, Dasman, Kuwait.
INSERM UMR-S1151, CNRS UMR-S8253, Institut Necker Enfants Malades, Université Paris Cité, Paris, France.

Thangavel Alphonse Thanaraj (TA)

Dasman Diabetes Institute, Dasman, Kuwait.

Heikki A Koistinen (HA)

Department of Medicine, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Department of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland.
Minerva Foundation Institute for Medical Research, Helsinki, Finland.

Jaakko Tuomilehto (J)

Department of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland.
Department of Public Health, University of Helsinki, Helsinki, Finland.

Fahd Al-Mulla (F)

Dasman Diabetes Institute, Dasman, Kuwait.

Rasheed Ahmad (R)

Dasman Diabetes Institute, Dasman, Kuwait.

Classifications MeSH