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饮食对SD大鼠肠道代谢产物及食欲控制因子的作用

Role of diet on intestinal metabolites and appetite control factors in SD rats.

作者信息

Lin Bo, Liu Yueming, Zhang Wei, Zou Wenli

机构信息

Department of Nephrology, Zhejiang Provincial People's Hospital, Hangzhou, 310014, P.R. China.

Department of Nephrology, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang 310014, P.R. China.

出版信息

Exp Ther Med. 2020 Sep;20(3):2665-2674. doi: 10.3892/etm.2020.8993. Epub 2020 Jul 13.

Abstract

The present study aimed to investigate changes in the levels of metabolites and appetite control factors caused by different dietary interventions in Sprague Dawley (SD) rats. A total of 35 male SD rats were weaned and immediately randomly assigned to five groups. The control group was given access to a normal chow diet, and the other groups received a high-fat diet (FAT group), high-sugar diet, high-fibre or high-protein diet (PRO group) for 4 weeks. The high-fat diet contributed to weight gain and adipose tissue formation, and affected lipid indexed. The FAT group had a higher body weight, Lee's index, adipose mass and glucose tolerance than all of the other groups. The opposite effect was observed in the PRO group. High-performance liquid chromatography revealed that short-chain fatty acid and amino acid formation were affected by the various diets. In addition, differences in the mRNA expression levels of leptin, ghrelin and associated receptors were determined in the gastrointestinal, adipose and hypothalamus tissues. The present study provides further evidence of the role of diet in obesity development and prevention. It also highlights the role of intestinal metabolites and appetite control factor expression in the pathogenesis of obesity in SD rats.

摘要

本研究旨在调查不同饮食干预对斯普拉格-道利(SD)大鼠代谢物水平和食欲控制因子的影响。总共35只雄性SD大鼠断奶后立即随机分为五组。对照组给予正常饲料饮食,其他组分别给予高脂饮食(FAT组)、高糖饮食、高纤维或高蛋白饮食(PRO组),持续4周。高脂饮食导致体重增加和脂肪组织形成,并影响脂质指标。FAT组的体重、李氏指数、脂肪量和葡萄糖耐量均高于其他所有组。而在PRO组观察到相反的效果。高效液相色谱显示,各种饮食会影响短链脂肪酸和氨基酸的形成。此外,还测定了胃肠道、脂肪和下丘脑组织中瘦素、胃饥饿素及相关受体的mRNA表达水平差异。本研究进一步证明了饮食在肥胖发生和预防中的作用。它还突出了肠道代谢物和食欲控制因子表达在SD大鼠肥胖发病机制中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b039/7401913/4b6a29d81489/etm-20-03-2665-g01.jpg

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