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赋予肥胖抵抗性并恢复瘦素缺陷肥胖小鼠的肠道屏障完整性。

Confers Obesity Resistance and Restores Intestinal Barrier Integrity in Leptin-deficient Obese Mice.

机构信息

Institute of Bioinformatics and Structural Biology, National Tsing Hua University, Hsinchu 30013, Taiwan.

Department of Medical Laboratory Science and Biotechnology, National Cheng Kung University, Tainan 70101, Taiwan.

出版信息

Nutrients. 2020 Mar 10;12(3):726. doi: 10.3390/nu12030726.

DOI:10.3390/nu12030726
PMID:32164196
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7146579/
Abstract

Obesity is associated with metabolic disorders. Thus, obesity prevention and treatment are essential for health. (AC) is a multifunctional medicinal fungus used for the treatment of various diseases and for preventing diet-induced obesity. Leptin deficiency causes over-eating and spontaneous obesity. The concomitant metabolic symptoms are more severe than diet-induced obesity. Here, we used leptin-deficient () mice as an animal model for over-feeding to study the effect of AC on obesity. We fed C57BL/6 mice (WT, ) and mice with AC for four weeks before performing qRT-PCR and immunoblot analysis to elaborate AC-modulated mechanisms. Further, we used Caco-2 cells as a human intestinal epithelial barrier model to examine the effect of AC on intestinal permeability. Our results suggested that AC reduces lipid deposits of the liver and epididymal white adipose tissue (EWAT) by promoting lipid metabolism and inhibiting lipogenesis-associated genes and proteins in mice. Moreover, AC effectively repaired intestinal-barrier injury caused by leptin deficiency and enhanced intestinal barrier integrity in Caco-2 cells. Interestingly, AC significantly reduced body weight and EWAT with no compromise on food intake in mice. Thus, AC effectively reduced obesity caused by leptin-deficiency and can potentially be used as a nutraceutical for treating obesity.

摘要

肥胖与代谢紊乱有关。因此,预防和治疗肥胖对于健康至关重要。(AC) 是一种多功能药用真菌,用于治疗各种疾病和预防饮食诱导的肥胖。瘦素缺乏会导致过度进食和自发性肥胖。伴随的代谢症状比饮食诱导的肥胖更为严重。在这里,我们使用瘦素缺乏 () 小鼠作为过食的动物模型,研究 AC 对肥胖的影响。我们用 AC 喂养 C57BL/6 小鼠 (WT, ) 和 小鼠四周,然后进行 qRT-PCR 和免疫印迹分析,阐述 AC 调节的机制。此外,我们使用 Caco-2 细胞作为人肠上皮屏障模型,研究 AC 对肠通透性的影响。我们的结果表明,AC 通过促进脂质代谢和抑制与脂肪生成相关的基因和蛋白,减少了 小鼠肝脏和附睾白色脂肪组织 (EWAT) 的脂质沉积。此外,AC 有效修复了由瘦素缺乏引起的肠道屏障损伤,并增强了 Caco-2 细胞中的肠道屏障完整性。有趣的是,AC 显著降低了 小鼠的体重和 EWAT,而不影响食物摄入。因此,AC 有效减轻了瘦素缺乏引起的肥胖,可以作为治疗肥胖的营养保健品。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f34/7146579/1269c9eb34b1/nutrients-12-00726-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f34/7146579/cbefa3173dcb/nutrients-12-00726-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f34/7146579/b81420429ec6/nutrients-12-00726-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f34/7146579/c169a572a772/nutrients-12-00726-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f34/7146579/72031bb2eab5/nutrients-12-00726-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f34/7146579/bdc062fa40e8/nutrients-12-00726-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f34/7146579/1269c9eb34b1/nutrients-12-00726-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f34/7146579/cbefa3173dcb/nutrients-12-00726-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f34/7146579/b81420429ec6/nutrients-12-00726-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f34/7146579/c169a572a772/nutrients-12-00726-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f34/7146579/72031bb2eab5/nutrients-12-00726-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f34/7146579/bdc062fa40e8/nutrients-12-00726-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f34/7146579/1269c9eb34b1/nutrients-12-00726-g006.jpg

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Upregulation of LGALS1 is associated with oral cancer metastasis.LGALS1的上调与口腔癌转移相关。
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