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A trans fatty acid substitute enhanced development of liver proliferative lesions induced in mice by feeding a choline-deficient, methionine-lowered, L-amino acid-defined, high-fat diet
Lipids in Health and Disease ( IF 4.5 ) Pub Date : 2020-12-14 , DOI: 10.1186/s12944-020-01423-3
Noriko Suzuki-Kemuriyama 1 , Akari Abe 2 , Kinuko Uno 3 , Shuji Ogawa 3 , Atsushi Watanabe 2 , Ryuhei Sano 2 , Megumi Yuki 2 , Katsuhiro Miyajima 1, 2 , Dai Nakae 1, 2
Affiliation  

Nonalcoholic 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. Mice 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. At 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(+). Replacement 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.

中文翻译:

一种反式脂肪酸替代品通过喂食缺乏胆碱、降低蛋氨酸、L-氨基酸确定的高脂肪饮食,促进小鼠肝脏增殖性病变的发展

非酒精性脂肪性肝炎 (NASH) 是一种以脂肪变性、坏死性炎症和纤维化为特征的肝脏疾病,可导致肝硬化和癌症。由于对人类健康的潜在危害和 NASH 风险的增加,努力集中在减少反式脂肪酸 (TFA) 的摄入量上。然而,减少膳食反式脂肪酸的健康益处尚未完全阐明。在这里,研究了 TFA 与替代品对通过喂养缺乏胆碱、降低蛋氨酸、L-氨基酸定义的高脂肪饮食 (CDAA-HF) 诱导的小鼠 NASH 的影响。给小鼠喂食含有 TFA 起酥油的 CDAA-HF (CDAA-HF-T(+))、含有不含 TFA 起酥油的 CDAA-HF (CDAA-HF-T(-)) 或对照食物 13 或 26 周。在第 13 周,通过喂食含有 TFA 的 CDAA-HF-T(+) 或不含 TFA 的 CDAA-HF-T(-) 在小鼠中诱导 NASH,但主要是饱和脂肪酸(FAs),血清转氨酶活性升高和肝脏变化(包括脂肪变性、炎症和纤维化)证明了这一点。CDAA-HF-T(-) 在第 13 周诱导更大程度的肝细胞凋亡。在第 26 周,在喂食 CDAA-HF-T(-) 的小鼠中,增殖性(肿瘤前和非肿瘤性)结节病变比 CDAA- 更明显HF-T(+)。至少在目前的情况下,用替代品替代膳食 TFA 促进了小鼠 NASH 模型肝脏中增殖病变的发展。应注意在人类消费食品中使用 TFA 替代品,并且 FA 的平衡可能比特定类型的 FA 更重要。包括脂肪变性、炎症和纤维化。CDAA-HF-T(-) 在第 13 周诱导更大程度的肝细胞凋亡。在第 26 周,在喂食 CDAA-HF-T(-) 的小鼠中,增殖性(肿瘤前和非肿瘤性)结节病变比 CDAA- 更明显HF-T(+)。至少在目前的情况下,用替代品替代膳食 TFA 促进了小鼠 NASH 模型肝脏中增殖病变的发展。应注意在人类消费食品中使用 TFA 替代品,并且 FA 的平衡可能比特定类型的 FA 更重要。包括脂肪变性、炎症和纤维化。CDAA-HF-T(-) 在第 13 周诱导更大程度的肝细胞凋亡。在第 26 周,在喂食 CDAA-HF-T(-) 的小鼠中,增殖性(肿瘤前和非肿瘤性)结节病变比 CDAA- 更明显HF-T(+)。至少在目前的情况下,用替代品替代膳食 TFA 促进了小鼠 NASH 模型肝脏中增殖病变的发展。应注意在人类消费食品中使用 TFA 替代品,并且 FA 的平衡可能比特定类型的 FA 更重要。与 CDAA-HF-T(+) 相比,喂食 CDAA-HF-T(-) 的小鼠的增殖性(肿瘤前和非肿瘤性)结节性病变更明显。至少在目前的情况下,用替代品替代膳食 TFA 促进了小鼠 NASH 模型肝脏中增殖病变的发展。应注意在人类消费食品中使用 TFA 替代品,并且 FA 的平衡可能比特定类型的 FA 更重要。与 CDAA-HF-T(+) 相比,喂食 CDAA-HF-T(-) 的小鼠的增殖性(肿瘤前和非肿瘤性)结节性病变更明显。至少在目前的情况下,用替代品替代膳食 TFA 促进了小鼠 NASH 模型肝脏中增殖病变的发展。应注意在人类消费食品中使用 TFA 替代品,并且 FA 的平衡可能比特定类型的 FA 更重要。
更新日期:2020-12-14
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