食品科学 ›› 2019, Vol. 40 ›› Issue (3): 149-157.doi: 10.7506/spkx1002-6630-20170807-093

• 营养卫生 • 上一篇    下一篇

鱼胶原蛋白肽对高脂膳食小鼠肝脏脂肪代谢和氧化还原状态的影响

田?许1,2,杨玉辉1,2,王雅楠1,2,张佳红1,2,郭海涛1,2,施用晖1,2,乐国伟1,2,*   

  1. (1.江南大学 食品科学与技术国家重点实验室,江苏?无锡 214122;2.江南大学食品学院,江苏?无锡 214122)
  • 出版日期:2019-02-15 发布日期:2019-03-05
  • 基金资助:
    国家自然科学基金面上项目(31172214);“十二五”国家科技支撑计划项目(2012BAD33B05)

Effects of Fish Collagen Peptides on Hepatic Lipid Metabolism and Redox Status in Mice Fed with High-Fat Diet

TIAN Xu1,2, YANG Yuhui1,2, WANG Yanan1,2, ZHANG Jiahong1,2, GUO Haitao1,2, SHI Yonghui1,2, LE Guowei1,2,*   

  1. (1. The State Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi 214122, China;2. School of Food Science and Technology, Jiangnan University, Wuxi 214122, China)
  • Online:2019-02-15 Published:2019-03-05

摘要: 目的:研究鱼胶原蛋白肽(fish collagen peptides,FCPs)对高脂膳食(high-fat diet,HFD)小鼠肝脏脂肪代谢和氧化还原状态的影响。方法:54?只C57BL/6雄性小鼠按体质量随机分为正常膳食组(CON)、HFD组(HF)和FCPs干预HFD组(PHF)。每周记录各组小鼠体质量,并按体质量把每组小鼠随机均分为两批,分别在第11和22周宰杀,测定采食量、脂肪表观消化率;肝脏中甘油三酯(triglyceride,TG)、总胆固醇和游离脂肪酸(free fatty acid,FFA)含量;肝脏脂代谢相关基因乙酰辅酶A羧化酶1、脂肪酸合成酶、固醇调节元件结合蛋白1c、胆固醇7α-羟化酶(cholesterol 7α-hydroxylase 1,CYP7A1)、过氧化物激活受体α(peroxisome proliferator activated receptor α,PPARα)和肉毒碱棕榈酰基转移酶1(carnitine palmity1 transferase 1,CPT1)的mRNA表达水平,肝脏氧化还原状态相关指标活性氧自由基(reactive oxygen species,ROS)、丙二醛、总抗氧化能力(total antioxidant capacity,T-AOC)、谷胱甘肽过氧化物酶(glutathion peroxidase,GSH-Px)活力和还原型/氧化型谷胱甘肽的水平。结果:第22周时,与HF组相比,PHF组小鼠的采食量、脂肪和能量摄入显著增加(P<0.05),肝脏的TG、FFA、脂肪空泡和脂肪浸润面积比明显降低(P<0.05),脂肪分解关键基因CYP7A1、PPARα和CPT1的mRNA表达水平显著上调(P<0.05),肝脏的ROS水平显著降低(P<0.05),T-AOC水平和GSH-Px活力显著升高(P<0.05)。结论:质量分数1% FCPs干预可能通过改善HFD小鼠肝脏氧化还原状态,促进肝脏脂肪分解代谢,起到减少小鼠肝脏脂肪蓄积和改善脂代谢。

关键词: 鱼胶原蛋白肽, 高脂膳食, 肝脏, 脂肪代谢, 氧化还原状态

Abstract: Objective: To investigate the effects of fish collagen peptides (FCPs) on hepatic lipid metabolism and redox status in mice fed with a high-fat diet (HFD). Methods: Male C57BL/6 mice (4 weeks old) were randomly divided into three groups (18 animals per group) based on body mass: including control normal diet (CON), high-fat diet (HF) and high-fat diet with 1% added FCPs (PHF) groups. Body mass was recorded on a weekly basis. The animals in each group were randomly assigned according to body mass into two groups which were sacrificed at the end of the 11th and 22th week, respectively. Average daily feed intake (ADFI) and apparent fat digestibility (AFD) were determined. Hepatic triglyceride (TG), total cholesterol (TC) and free fatty acid (FFA) were examined. The mRNA expression levels of key regulators of hepatic lipid metabolism such as acety1 CoA-carboxylase 1 (ACC-1), fatty acid synthase (FAS), sterol regulatory element-binding protein 1c (SREBP1c), cholesterol 7α-hydroxylase 1 (CYP7A1), peroxisome proliferator activated receptor α (PPARα) and carnitine palmity1 transferase 1 (CPT1) were analyzed by quantitative real-time polymerase chain reaction (qPCR). The levels of hepatic redox status indicators such as reactive oxygen species (ROS), malondialdehyde (MDA), total antioxidant capacity (T-AOC), glutathione peroxidase (GSH-Px) and ratio of reduced to oxidized glutathione (GSH/GSSG) were determined. Results: After 22 weeks, in comparison to the HF group, the PHF group showed significantly increased levels of ADFI, fat and energy intake (P < 0.05). The concentrations of hepatic TG and FFA, and the ratios of adipose vacuoles and infiltration area were markedly decreased in the PHF group (P < 0.05). The mRNA expression of CYP7A1, PPARα and CPT1 in liver was significantly up-regulated in the PHF group (P < 0.05). Meanwhile, FCPs improved the redox status due to markedly decreased hepatic ROS (P < 0.05), and significantly increased T-AOC and GSH-Px (P < 0.05). Conclusion: Dietary intervention with 1% FCP can markedly decrease fat accumulation in liver and regulate liver lipid metabolism by improving hepatic redox status and accelerating lipid catabolism in HFD-fed mice.

Key words: fish collagen peptides (FCPs), high-fat diet (HFD), liver, lipid metabolism, redox status

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