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膳食补充多糖通过调节炎症反应和脂质代谢减轻小鼠营养性肥胖。

Dietary Supplementation of Polysaccharides Alleviate Nutritional Obesity in Mice via Regulating Inflammatory Response and Lipid Metabolism.

作者信息

Liu Qian, Ma Ruisen, Li Si, Fei Yujie, Lei Jing, Li Ruoyu, Pan Yu, Liu Sining, Wang Langhong

机构信息

College of Food Science and Technology, Northwest University, Xi'an 710069, China.

出版信息

Foods. 2022 Mar 24;11(7):942. doi: 10.3390/foods11070942.

DOI:10.3390/foods11070942
PMID:35407029
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8997552/
Abstract

The incidence of lipid metabolism disorder and obesity that is caused by high-calorie diets is increasing year by year, which has become an urgent global health problem. This study was performed to explore the intervention effects of polysaccharides that were extracted from resources in the Qinba Mountain area on nutritional obesity in C57BL/6J mice that was induced by high fat and high fructose diets (HFFD) and to investigate their underlying molecular mechanisms. The results showed that dietary supplementation of polysaccharides (AAP) significantly improved mice's insulin resistance state, altered serum lipid metabolites, and slowed down body weight gain that was induced by HFFD. In addition, AAP supplementation decreased inflammatory factor levels and alleviated liver histomorphology changes. Furthermore, AAP down-regulated liver adipogenic-related gene expressions, suppressed cholesterol synthesis-related gene levels, up-regulated fatty acid β-oxidation-related gene expressions, and promoted cholesterol efflux-related gene expressions, thus improving mice hepatic lipid metabolism homeostasis. Moreover, the intervention effects were closely related to mitochondrial function. These results provide a scientific basis for the further development and utilization of resources in the Qinba Mountain area.

摘要

由高热量饮食导致的脂质代谢紊乱和肥胖的发病率逐年上升,这已成为一个紧迫的全球健康问题。本研究旨在探讨从秦巴山区资源中提取的多糖对高脂高糖饮食(HFFD)诱导的C57BL/6J小鼠营养性肥胖的干预作用,并研究其潜在的分子机制。结果表明,膳食补充多糖(AAP)显著改善了小鼠的胰岛素抵抗状态,改变了血清脂质代谢物,并减缓了HFFD诱导的体重增加。此外,补充AAP降低了炎症因子水平,减轻了肝脏组织形态学变化。此外,AAP下调了肝脏脂肪生成相关基因的表达,抑制了胆固醇合成相关基因的水平,上调了脂肪酸β-氧化相关基因的表达,并促进了胆固醇流出相关基因的表达,从而改善了小鼠肝脏脂质代谢稳态。此外,干预效果与线粒体功能密切相关。这些结果为秦巴山区资源的进一步开发利用提供了科学依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1af9/8997552/dde65f364d2e/foods-11-00942-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1af9/8997552/08cc0ec293ae/foods-11-00942-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1af9/8997552/fc90ada0ffe9/foods-11-00942-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1af9/8997552/3fd39c2f8558/foods-11-00942-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1af9/8997552/1bf7d97a42c9/foods-11-00942-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1af9/8997552/ccf620e0d93e/foods-11-00942-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1af9/8997552/7c336e23fce1/foods-11-00942-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1af9/8997552/3d0caa94a569/foods-11-00942-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1af9/8997552/dde65f364d2e/foods-11-00942-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1af9/8997552/08cc0ec293ae/foods-11-00942-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1af9/8997552/fc90ada0ffe9/foods-11-00942-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1af9/8997552/3fd39c2f8558/foods-11-00942-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1af9/8997552/1bf7d97a42c9/foods-11-00942-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1af9/8997552/ccf620e0d93e/foods-11-00942-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1af9/8997552/7c336e23fce1/foods-11-00942-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1af9/8997552/3d0caa94a569/foods-11-00942-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1af9/8997552/dde65f364d2e/foods-11-00942-g008.jpg

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