TY - JOUR
T1 - sunflower oil hfd feeding in mice leads to gut dysbiosis, mild steatohepatitis, and impaired glycemic control
AU - Sindhu, Sardar T. A. K.
AU - Bahman, Fatemah
AU - Malik, Mohammad Zubbair
AU - Arefanian, Hossein
AU - Alrashed, Fatema
AU - Nizam, Rasheeba
AU - Kochumon, Shihab P.
AU - Thomas, Reeby S.
AU - Albeloushi, Shaima
AU - Hasan, Amal
AU - Abu-Farha, Mohamed
AU - Al Madhoun, Ashraf
AU - Thangavel, Alphonse T.
AU - Almulla, Fahd
AU - Ahmad, Rasheed
PY - 2024
Y1 - 2024
N2 - Introduction & Objective: High-fat diets (HFDs) influence gut microbiota and promote obesity & metabolic dysregulation. Dietary sucrose is a co-player in modifying gut microbial ecosystem towards dysbiosis. Fish & sunflower dietary fats may be consumed with/without sucrose; however, gut bacterial changes from excessive intake of these fats, without the added effect of sucrose, remain unclear. Methods: To address this objective, we compared effects of sucrose-free, sunflower high-fat diet (S-HFD) & fish (F)-HFD feeding (24 wks) on the gut microbiota, obesity, liver inflammation, and glycemic control in C57BL/6 mice. Results: The 16S rRNA sequencing of fecal microbiome showed that gut bacterial communities were differentially expressed between two dietary groups. Firmicutes were highly-abundant in S-HFD (40%) compared to F-HFD (3%) mice, while Verrucomicrobia were abundant in F-HFD (26%) compared to S-HFD (˂1%) mice. Firmicutes/Bacteroidetes ratios in S-HFD & F-HFD were 1.32 & 2.45, respectively. MicrobiomeAnalyst & MIAOME analyses identified highly-abundant taxa in S-HFD mice, including Oscillospira, guilliermondii, Allobaculum, Yaniella, Ruminococcus, gnavus, Staphylococcus, Clostridium, Adlercreutzia, Aerococcaceae, Anaeroplasma, Mogibacteriaceae, Christensenellaceae, & RF39, having predicted associations with host genes of metabolic disorders/pathways linked to inflammation & glucose metabolism. Compared to F-HFD mice, the S-HFD mice showed slightly increased body weights (P = 0.06) but significant differences regarding fasting hyperglycemia, hepatic macrophage infiltration (F4/80 expression), macrovascular steatosis, lobular inflammation, & expression of genes associated with de novo lipogenesis (Acaca, Fasn, and Scd1) & monocyte chemotaxis (Ccl2). Conclusion: Taken together, S-HFD feeding in mice leads to gut dysbiosis and the clinical manifestations of moderate liver inflammation, steatosis and impaired glycemic control. Disclosure S.T. Sindhu: None. F. Bahman: None. M. Malik: None. H. Arefanian: None. F. Alrashed: None. R. Nizam: None. S.P. Kochumon: None. R.S. Thomas: None. S. Albeloushi: None. A. Hasan: None. M. Abu-farha: None. A. Al Madhoun: None. A.T. Thangavel: None. F. Almulla: None. R. Ahmad: None. Funding Kuwait Foundation for the Advancement of Sciences (KFAS) (Grants #: RA 2010-003)
AB - Introduction & Objective: High-fat diets (HFDs) influence gut microbiota and promote obesity & metabolic dysregulation. Dietary sucrose is a co-player in modifying gut microbial ecosystem towards dysbiosis. Fish & sunflower dietary fats may be consumed with/without sucrose; however, gut bacterial changes from excessive intake of these fats, without the added effect of sucrose, remain unclear. Methods: To address this objective, we compared effects of sucrose-free, sunflower high-fat diet (S-HFD) & fish (F)-HFD feeding (24 wks) on the gut microbiota, obesity, liver inflammation, and glycemic control in C57BL/6 mice. Results: The 16S rRNA sequencing of fecal microbiome showed that gut bacterial communities were differentially expressed between two dietary groups. Firmicutes were highly-abundant in S-HFD (40%) compared to F-HFD (3%) mice, while Verrucomicrobia were abundant in F-HFD (26%) compared to S-HFD (˂1%) mice. Firmicutes/Bacteroidetes ratios in S-HFD & F-HFD were 1.32 & 2.45, respectively. MicrobiomeAnalyst & MIAOME analyses identified highly-abundant taxa in S-HFD mice, including Oscillospira, guilliermondii, Allobaculum, Yaniella, Ruminococcus, gnavus, Staphylococcus, Clostridium, Adlercreutzia, Aerococcaceae, Anaeroplasma, Mogibacteriaceae, Christensenellaceae, & RF39, having predicted associations with host genes of metabolic disorders/pathways linked to inflammation & glucose metabolism. Compared to F-HFD mice, the S-HFD mice showed slightly increased body weights (P = 0.06) but significant differences regarding fasting hyperglycemia, hepatic macrophage infiltration (F4/80 expression), macrovascular steatosis, lobular inflammation, & expression of genes associated with de novo lipogenesis (Acaca, Fasn, and Scd1) & monocyte chemotaxis (Ccl2). Conclusion: Taken together, S-HFD feeding in mice leads to gut dysbiosis and the clinical manifestations of moderate liver inflammation, steatosis and impaired glycemic control. Disclosure S.T. Sindhu: None. F. Bahman: None. M. Malik: None. H. Arefanian: None. F. Alrashed: None. R. Nizam: None. S.P. Kochumon: None. R.S. Thomas: None. S. Albeloushi: None. A. Hasan: None. M. Abu-farha: None. A. Al Madhoun: None. A.T. Thangavel: None. F. Almulla: None. R. Ahmad: None. Funding Kuwait Foundation for the Advancement of Sciences (KFAS) (Grants #: RA 2010-003)
U2 - 10.2337/db24-1600-P
DO - 10.2337/db24-1600-P
M3 - Article
SN - 0012-1797
VL - 73
JO - Diabetes
JF - Diabetes
ER -