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A mouse model of short‐term, diet‐induced fatty liver with abnormal cardiolipin remodeling via downregulated Tafazzin gene expression
Author(s) -
Sakurai Toshihiro,
Chen Zhen,
Yamahata Arisa,
Hayasaka Takahiro,
Satoh Hiroshi,
Sekiguchi Hirotaka,
Chiba Hitoshi,
Hui ShuPing
Publication year - 2021
Publication title -
journal of the science of food and agriculture
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 142
eISSN - 1097-0010
pISSN - 0022-5142
DOI - 10.1002/jsfa.11144
Subject(s) - cardiolipin , mitochondrion , medicine , endocrinology , chemistry , biochemistry , biology , phospholipid , membrane
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