• Eri Nanizawa, Shun Otsuka, Naoyuki Hatayama, Yuki Tamaki, Yumi Hayashi, Tetsuya Ishikawa, Shuichi Hirai, and Munekazu Naito.
• Department of Anatomy, Aichi Medical University, Nagakute-city, Aichi, Japan. Electronic address: nanizawa.e@aichi-med-u.ac.jp.
• Nutrition. 2022 Sep 1; 101: 111710.

ObjectivesHigh-fat diet (HFD) and high-carbohydrate diet (HCD) are strongly linked to nonalcoholic fatty liver disease, a hepatic manifestation of metabolic syndrome. The mechanism of pathologic progression from nonalcoholic fatty liver disease to nonalcoholic steatohepatitis, which is a more severe form associated with inflammation and fibrosis, remains poorly understood. Thus, the aim of this study was to investigate and compare the inflammatory and coagulative state of the liver in short-term HFD- or HCD-fed mice with acute liver injury induced by concanavalin A (Con A).MethodsHistopathologic evaluation, real-time polymerase chain reaction, and immunohistochemical evaluation were performed on the liver of mice fed HFDs and HCDs for 4 d before and after Con A administration.ResultsThe liver of the HFD-fed mice had larger fibrinogen/fibrin depositions than those fed the HCD. HCD induced the expression of the proinflammatory cytokine tumor necrosis factor-α in the liver. Moreover, the expression of proinflammatory cytokines and chemokines was further enhanced after Con A stimulation in HCD (e.g., interleukin-1α, interleukin-6 at 1 h), with a strong tendency for inflammatory cell infiltration also found (24 h).ConclusionsShort-term HCD and HFD increased susceptibility to liver injury. HCD tended to induce more intense inflammation, whereas HFD tended to induce more intense hypercoagulation, suggesting that HCD and HFD may have different mechanisms of pathologic progression to nonalcoholic steatohepatitis.Copyright © 2022 Elsevier Inc. All rights reserved.

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