Department of Nutritional Sciences, University of Connecticut, Storrs, CT 06269, USA.
Department of Food and Nutrition, Changwon National University, Changwon 51140, Korea.
Nutrients. 2022 May 29;14(11):2280. doi: 10.3390/nu14112280.
Fucoxanthin (FCX) is a xanthophyll carotenoid present in brown seaweed. The goal of this study was to examine whether FCX supplementation could attenuate obesity-associated metabolic abnormalities, fibrosis, and inflammation in two diet-induced obesity (DIO) mouse models. C57BL/6J mice were fed either a high-fat/high-sucrose/high-cholesterol (HFC) diet or a high-fat/high-sucrose (HFS) diet. The former induces more severe liver injury than the latter model. In the first study, male C57BL/6J mice were fed an HFC diet, or an HFC diet containing 0.015% or 0.03% (/) FCX powder for 12 weeks to develop obesity-induced nonalcoholic steatohepatitis (NASH). In the second study, mice were fed an HFS diet or an HFS diet containing 0.01% FCX powder for 8 weeks. FCX did not change body weight gain and serum lipid profiles compared to the HFC or HFS controls. No significant differences were present in liver triglyceride and total cholesterol, hepatic fat accumulation, and serum alanine aminotransferase levels between control and FCX-fed mice regardless of whether they were on an HFC or HFS diet. FCX did not mitigate mRNA abundance of genes involved in lipid synthesis, cholesterol metabolism, inflammation, and fibrosis in the liver and white adipose tissue, while hepatic fatty acid β-oxidation genes were significantly elevated by FCX in both HFC and HFS feeding studies. Additionally, in the soleus muscle, FCX supplementation significantly elevated genes that regulate mitochondrial biogenesis and fatty acid β-oxidation, concomitantly increasing mitochondrial DNA copy number, compared with HFC. In summary, FCX supplementation had minor effects on hepatic and white adipose inflammation and fibrosis in two different DIO mouse models.
褐藻多酚（FCX）是一种存在于褐藻中的叶黄素类胡萝卜素。本研究旨在探讨 FCX 补充剂是否能减轻两种饮食诱导肥胖（DIO）小鼠模型中与肥胖相关的代谢异常、纤维化和炎症。C57BL/6J 小鼠分别喂食高脂肪/高蔗糖/高胆固醇（HFC）饮食或高脂肪/高蔗糖（HFS）饮食。前者比后者模型诱导更严重的肝损伤。在第一项研究中，雄性 C57BL/6J 小鼠喂食 HFC 饮食或 HFC 饮食，添加 0.015%或 0.03%（/）褐藻多酚粉 12 周，以诱发肥胖诱导的非酒精性脂肪性肝炎（NASH）。在第二项研究中，小鼠喂食 HFS 饮食或 HFS 饮食，添加 0.01%褐藻多酚粉 8 周。与 HFC 或 HFS 对照组相比，褐藻多酚并未改变体重增加和血脂谱。无论喂食 HFC 还是 HFS 饮食，褐藻多酚喂养的小鼠的肝甘油三酯和总胆固醇、肝脂肪堆积和血清丙氨酸氨基转移酶水平均无显著差异。褐藻多酚并未减轻肝脏和白色脂肪组织中与脂质合成、胆固醇代谢、炎症和纤维化相关的基因的 mRNA 丰度，而在 HFC 和 HFS 喂养研究中，肝脏脂肪酸β-氧化基因的丰度显著升高。此外，在比目鱼肌中，褐藻多酚补充显著增加了调节线粒体生物发生和脂肪酸β-氧化的基因，同时增加了线粒体 DNA 拷贝数，与 HFC 相比。总之，褐藻多酚补充对两种不同的 DIO 小鼠模型中的肝和白色脂肪炎症和纤维化仅有轻微影响。
