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短链壳聚糖对饮食诱导肥胖小鼠的抗肥胖作用

Antiobesity Effects of Short-Chain Chitosan in Diet-Induced Obese Mice.

作者信息

Do Ah Ra, Cho Su-Jung, Cho Yun-Young, Kwon Eun-Young, Choi Ji-Young, Lee Jeong Hyeon, Han Youngji, Kim Yi Soo, Piao Zhe, Shin Yong Chul, Choi Myung-Sook

机构信息

1 Department of Food Science and Nutrition, Daegu, Republic of Korea.

2 Center for Food and Nutritional Genomics Research, Kyungpook National University , Daegu, Republic of Korea.

出版信息

J Med Food. 2018 Sep;21(9):927-934. doi: 10.1089/jmf.2017.4115. Epub 2018 Sep 5.

Abstract

Dietary chitosan is known for its antiobesity effects by combining with bile acid and lipid droplets. When the chitosan structure is broken into short chains, the fat-binding capacity increases. The aim of this study was to compare long-chain chitosan (LC) with short-chain chitosan (SC) for their antiobesity effects in high-fat diet (HFD)-induced obese C57BL/6J mice for 12 weeks. The body weights of mice in both chitosan groups were decreased, especially in the SC group compared with the LC group. Total white adipose tissue and visceral fat weights were also decreased in mice of the SC group more than those of the HFD group. Moreover, SC supplementation lowered plasma triglyceride (TG) and cholesterol levels, whereas LC only lowered plasma free fatty acid level. Fecal lipids were increased in mice of both LC and SC groups, and hepatic TG and cholesterol levels were decreased in both groups. SC lowered phosphatidate phosphohydrolase activity and elevated β-oxidation in the liver. Furthermore, SC decreased the expression of the hepatic lipid-regulating genes, including fatty acid synthase, peroxisome proliferator-activated receptor (PPAR)γ1, and PPARγ2; and increased the expression of carnitine palmitoyl transferase 1α and peroxisome proliferator-activated receptor γ coactivator (PGC)1α genes. In conclusion, we demonstrated that long-term supplementation of SC can ameliorate body weight and lipid levels by increasing lipid excretion and regulating lipid metabolism, including some enzyme activities and gene expression levels, in HFD-induced obese mice.

摘要

膳食壳聚糖因其与胆汁酸和脂滴结合的抗肥胖作用而闻名。当壳聚糖结构分解为短链时,其脂肪结合能力增强。本研究旨在比较长链壳聚糖(LC)和短链壳聚糖(SC)对高脂饮食(HFD)诱导的肥胖C57BL/6J小鼠进行12周干预后的抗肥胖效果。两个壳聚糖组小鼠的体重均有所下降,尤其是SC组与LC组相比。SC组小鼠的总白色脂肪组织和内脏脂肪重量也比HFD组下降得更多。此外,补充SC可降低血浆甘油三酯(TG)和胆固醇水平,而LC仅降低血浆游离脂肪酸水平。LC组和SC组小鼠的粪便脂质均增加,两组的肝脏TG和胆固醇水平均降低。SC降低了肝脏中磷脂酸磷酸水解酶的活性并提高了β-氧化。此外,SC降低了肝脏脂质调节基因的表达,包括脂肪酸合酶、过氧化物酶体增殖物激活受体(PPAR)γ1和PPARγ2;并增加了肉碱棕榈酰转移酶1α和过氧化物酶体增殖物激活受体γ共激活因子(PGC)1α基因的表达。总之,我们证明了长期补充SC可以通过增加脂质排泄和调节脂质代谢(包括一些酶活性和基因表达水平)来改善HFD诱导的肥胖小鼠的体重和脂质水平。

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