Soy Protein Isolate Suppresses Lipodystrophy-induced Hepatic Lipid Accumulation in Model Mice
Soy Protein Isolate Suppresses Lipodystrophy-induced Hepatic Lipid Accumulation in Model Mice
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DOI：
10.5650/jos.ess16145
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发表时间：
2017-02-01
影响因子：
1.5
通讯作者：
Yanagita, Teruyoshi
中科院分区：
文献类型：
--
作者：
Nagao, Koji;Matsumoto, Akiko;Yanagita, Teruyoshi
脂肪代谢障碍是获得性和遗传性疾病，其特征在于完全或部分缺乏体脂，伴有一系列代谢疾病，包括肝脂肪变性。由于大豆分离蛋白（SPI）已被报道可以降低动物和人类的胆固醇和甘油三酯水平，我们探讨了SPI对饮食诱导的脂肪代谢障碍模型小鼠肝脏脂质代谢的病理生理学影响。四周的脂肪营养不良模型饮食诱导小鼠肝脏脂质积聚，伴随着脂肪组织和血清脂肪细胞因子的显著缺乏。然而，在脂肪代谢障碍模型饲料中添加SPI可以在不影响饲料脂肪萎缩效果的情况下减轻肝脏脂肪积聚。在该模型中，脂肪生成增强是肝脏脂肪变性的主要机制，但SPI补充显著减弱了酶活性和/或mRNA表达的增加。此外，SPI补充上调参与胆固醇代谢酶的肝脏mRNA表达。总之，我们的研究结果表明，膳食SPI可以通过直接减少肝脏脂肪生成而不影响脂肪细胞因子的产生来减轻脂代谢障碍诱导的肝脏脂肪变性。
Lipodystrophies are acquired and genetic disorders characterized by the complete or partial absence of body fat with a line of metabolic disorders, including hepatic steatosis. Because soy protein isolate (SPI) has been reported to reduce cholesterol and triglyceride levels in animals and humans, we explored the effect of SPI on the pathophysiology of hepatic lipid accumutaion in a diet-induced lipodystrophy model mice. Four weeks of the lipodystrophy model diet induced hepatic lipid accumulation concomitant with marked deficiencies of adipose tissue and serum adipocytokines in mice. However, supplementing the lipodystrophy model diet with SPI could alleviate the hepatic lipid acculation without affecting the lipoatrophic effect of the diet. Enhanced lipogenesis is the principal mechanism of hepatic steatosis in this model, but SPI supplementation significantly attenuated the increase in enzyme activity and/or mRNA expression. Additionally, SPI supplementation upregulated the hepatic mRNA expression of an enzyme involved in cholesterol catabolism. In conclusion, our results indicate the possibility of dietary SPI to attenuate lipodystorophy-induced hepatic steatosis through the direct reduction of hepatic lipogenesis without affecting adipocytokine production.