Abstract
BackgroundNonalcoholic steatohepatitis (NASH) is a form of liver disease characterized by steatosis, necroinflammation, and fibrosis, resulting in cirrhosis and cancer. Efforts have focused on reducing the intake of trans fatty acids (TFAs) because of potential hazards to human health and the increased risk for NASH. However, the health benefits of reducing dietary TFAs have not been fully elucidated. Here, the effects of TFAs vs. a substitute on NASH induced in mice by feeding a choline-deficient, methionine-lowered, L-amino acid-defined, high-fat diet (CDAA-HF) were investigated.MethodsMice were fed CDAA-HF containing shortening with TFAs (CDAA-HF-T(+)), CDAA-HF containing shortening without TFAs (CDAA-HF-T(−)), or a control chow for 13 or 26 weeks.ResultsAt week 13, NASH was induced in mice by feeding CDAA-HF-T(+) containing TFAs or CDAA-HF-T(−) containing no TFAs, but rather mostly saturated fatty acids (FAs), as evidenced by elevated serum transaminase activity and liver changes, including steatosis, inflammation, and fibrosis. CDAA-HF-T(−) induced a greater extent of hepatocellular apoptosis at week 13. At week 26, proliferative (preneoplastic and non-neoplastic) nodular lesions were more pronounced in mice fed CDAA-HF-T(−) than CDAA-HF-T(+).ConclusionsReplacement of dietary TFAs with a substitute promoted the development of proliferation lesions in the liver of a mouse NASH model, at least under the present conditions. Attention should be paid regarding use of TFA substitutes in foods for human consumption, and a balance of FAs is likely more important than the particular types of FAs.
Highlights
Nonalcoholic steatohepatitis (NASH) is a form of liver disease characterized by steatosis, necroinflammation, and fibrosis, resulting in cirrhosis and cancer
The aim of the present study is to comparably investigate the effects of shortenings with and without Trans fatty acid (TFA) on NASH induced in mice by feeding our original high-fat CDAA (CDAA-HF), and to assess the safety concerns associated with the use of TFA substitutes
In conclusion, the replacement of dietary TFAs with a substitute aggravated the development of liver proliferative lesions nutritionally induced NASH in mice, at least under the present conditions
Summary
Nonalcoholic steatohepatitis (NASH) is a form of liver disease characterized by steatosis, necroinflammation, and fibrosis, resulting in cirrhosis and cancer. Nonalcoholic steatohepatitis (NASH) is a form of liver disease characterized by steatosis, inflammation, ballooning, and subsequent death of hepatocytes. It is associated with hepatic fibrosis, resulting in cirrhosis and cancer [1,2,3]. Inflammation activates a stress response, resulting in a wide variety of injuries to hepatocytes, including lipidosis, resulting in hepatocellular lipid accumulation (i.e., steatosis) and the subsequent onset of NASH [5,6,7,8]. Various factors, including toxic lipids, nutrients, and other macrophage- and adipose-derived signals, may induce inflammatory insults
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