Lotus seed resistant starch ameliorates high-fat diet induced hyperlipidemia by fatty acid degradation and glycerolipid metabolism pathways in mouse liver

高脂血症 内科学 脂质代谢 脂肪酸代谢 脂肪酸 脂肪变性 内分泌学 脂肪肝 甘油三酯 生物 新陈代谢 生物化学 胆固醇 化学 医学 糖尿病 疾病
作者
Shuqi He,Zixiao Xiong,Lanxin Li,Yanbo Wang,Chong Wang,Baodong Zheng,Hongliang Zeng,Yi Zhang
出处
期刊:International Journal of Biological Macromolecules [Elsevier BV]
卷期号:215: 79-91 被引量:24
标识
DOI:10.1016/j.ijbiomac.2022.06.077
摘要

We investigated the potential efficacy and underlying mechanisms of Lotus seed Resistant Starch (LRS) for regulating hyperlipidemia in mice fed a High-fat Diet (HFD). Mouse were fed a normal diet (Normal Control group, NC group), HFD alone (MC group), HFD plus lovastatin (PC group), or HFD with low/medium/high LRS (LLRS, MLRS, and HLRS groups, respectively) for 4 weeks. LRS supplementation significantly decreased body weight and significantly reduced serum levels of total cholesterol, triglycerides, low-density lipoprotein cholesterol, and high-density lipopro-tein cholesterol compared with the MC group. LRS also significantly alleviated hepatic steatosis, especially in the MLRS group, which also showed a significantly reduced visceral fat index. LLRS supplementation significantly regulated genes associated with glycerolipid metabolism and steroid hormone biosynthesis (Lpin1 and Ugt2b38), MLRS significantly regulated genes related to fatty acid degradation, fatty acid elongation, and glycerolipid metabolism (Lpin1, Hadha, Aldh3a2, and Acox1), whereas HLRS significantly regulated genes related to fatty acid elongation and glycerolipid metabolism (Lpin1, Elovl3, Elovol5, and Agpat3). The fatty acid-degradation pathway regulated by MLRS thus exerts better control of serum lipid levels, body weight, visceral fat index, and liver steatosis in mice compared with LLRS- and HLRS-regulated pathways.
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