A mouse model of short‐term, diet‐induced fatty liver with abnormal cardiolipin remodeling via downregulated Tafazzin gene expression. (12th March 2021)

• Record Type: Journal Article
• Authors: Sakurai, Toshihiro; Chen, Zhen; Yamahata, Arisa; Hayasaka, Takahiro; Satoh, Hiroshi; Sekiguchi, Hirotaka; Chiba, Hitoshi; Hui, Shu‐Ping
• Is Part Of: Journal of the science of food and agriculture. Volume 101:Number 12(2021)
• Page Start: 4995
• Page End: 5001
• Publication Date: 2021-03-12
• Subjects: high‐carbohydrate diet -- liquid chromatography mass spectrometry -- lipidomics -- mitochondria -- monolysocardiolipin; Food -- Periodicals; Agriculture -- Periodicals; 664
• DOI: 10.1002/jsfa.11144
• Languages: English
• ISSNs: 0022-5142

Abstract

Abstract: Background: Cardiolipin (CL) helps maintain mitochondrial structure and function. Here we investigated whether a high carbohydrate diet (HCD) fed to mice for a short period (5 days) could modulate the CL level, including that of monolysoCL (MLCL) in the liver. Results: Total CL in the HCD group was 22% lower than that in the normal chow diet (NCD) group ( P < 0.05). The CL72:8 level strikingly decreased by 93% ( P < 0.0001), whereas total nascent CLs (CLs other than CL72:8) increased ( P < 0.01) in the HCD group. The total MLCL in the HCD group increased by 2.4‐fold compared with that in the NCD group ( P < 0.05). Tafazzin expression in the HCD group was significantly downregulated compared with that in the NCD group ( P < 0.05). A strong positive correlation between nascent CL and total MLCL (r = 0.955, P < 0.0001), and a negative correlation between MLCL and Tafazzin expression (r = −0.593, P = 0.0883) were observed. Conclusion: A HCD modulated the fatty acid composition of CL and MLCL via Tafazzin in the liver, which could lead to mitochondrial dysfunction. This model may be useful for elucidating the relationship between fatty liver and mitochondrial dysfunction. © 2021 Society of Chemical Industry