首页> 美国卫生研究院文献>International Journal of Molecular Sciences >Effects and Mechanisms of Chitosan and ChitosanOligosaccharide on Hepatic Lipogenesis and Lipid Peroxidation Adipose Lipolysis and Intestinal Lipid Absorption in Rats with High-Fat Diet-Induced Obesity
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Effects and Mechanisms of Chitosan and ChitosanOligosaccharide on Hepatic Lipogenesis and Lipid Peroxidation Adipose Lipolysis and Intestinal Lipid Absorption in Rats with High-Fat Diet-Induced Obesity

机译:壳聚糖和壳藻糖苷对高脂饮食肥胖症大鼠肝脂肪发生和脂质过氧化脂质过氧化脂质脂解和肠脂吸收的影响及机制

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摘要

Chitosan and its derivative, chitosan oligosaccharide (CO), possess hypolipidemic and anti-obesity effects. However, it is still unclear if the mechanisms are different or similar between chitosan and CO. This study was designed to investigate and compare the effects of CO and high-molecular-weight chitosan (HC) on liver lipogenesis and lipid peroxidation, adipose lipolysis, and intestinal lipid absorption in high-fat (HF) diet-fed rats for 12 weeks. Rats were divided into four groups: normal control diet (NC), HF diet, HF diet+5% HC, and HF diet+5% CO. Both HC and CO supplementation could reduce liver lipid biosynthesis, but HC had a better effect than CO on improving liver lipid accumulation in HF diet-fed rats. The increased levels of triglyceride decreased lipolysis rate, and increased lipoprotein lipase activity in the perirenal adipose tissue of HF diet-fed rats could be significantly reversed by both HC and CO supplementation. HC, but not CO, supplementation promoted liver antioxidant enzymes glutathione peroxidase and superoxide dismutase activities and reduced liver lipid peroxidation. In the intestines, CO, but not HC, supplementation reduced lipid absorption by reducing the expression of fabp2 and fatp4 mRNA. These results suggest that HC and CO have different mechanisms for improving lipid metabolism in HF diet-fed rats.
机译:壳聚糖及其衍生物,壳聚糖寡糖(CO),具有低血脂和抗肥胖作用。然而,如果机制在壳聚糖和CO之间的机制是不同的或类似的机制尚不清楚。本研究旨在研究和比较CO和高分子量壳聚糖(HC)对肝脂肪生成和脂质过氧化,脂肪脂解的影响,在高脂肪(HF)饮食喂养大鼠中的肠道脂肪吸收12周。大鼠分为四组:正常对照饮食(NC),HF饮食,HF饮食+ 5%HC,以及HF饮食+ 5%CO。HC和CO补充可以降低肝脂生物合成,但HC效果更好提高HF饮食饲料大鼠肝脏脂质积累的CO.脂溶解率的增加程度增加,HF饮食大鼠的肝癌脂肪酶脂肪酶活性增加,HC和CO补充可能会显着逆转。 HC,但不是CO,补充促进肝脏抗氧化酶谷胱甘肽过氧化物酶和超氧化物歧化酶活性和降低的肝脂质过氧化。在肠道中,CO,但不是HC,补充通过减少Fabp2和FATP4 mRNA的表达来减少脂质吸收。这些结果表明,HC和CO具有不同的机制,用于改善HF饮食喂养大鼠的脂质代谢。

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