• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

嗜酸乳杆菌 263 与高能饮食喂养大鼠白色脂肪组织能量代谢重塑相关的抗肥胖作用。

Antiobesity effect of Lactobacillus reuteri 263 associated with energy metabolism remodeling of white adipose tissue in high-energy-diet-fed rats.

机构信息

YongLin Biomedical Engineering Center, National Taiwan University, Taipei City 10617, Taiwan.

Research and Development Department, GenMont Biotech Incorporation, Tainan 741, Taiwan.

出版信息

J Nutr Biochem. 2018 Apr;54:87-94. doi: 10.1016/j.jnutbio.2017.11.004. Epub 2017 Nov 16.

DOI:10.1016/j.jnutbio.2017.11.004
PMID:29329013
Abstract

Obesity is a serious and costly issue to the medical welfare worldwide. Probiotics have been suggested as one of the candidates to resolve the obesity-associated problems, but how they combat obesity is not fully understood. Herein, we investigated the effects of Lactobacillus reuteri 263 (L. reuteri 263) on antiobesity using four groups of Sprague-Dawley rats (n=10/group), namely, C (normal diet with vehicle treatment), HE [high-energy diet (HED) with vehicle treatment], 1X (HED with 2.1×10 CFU/kg/day of L. reuteri 263) and 5X (HED with 1.05×10 CFU/kg/day of L. reuteri 263), for 8 weeks. L. reuteri 263 improved the phenomenon of obesity, serum levels of proinflammatory factors and antioxidant enzymes. More importantly, L. reuteri 263 increased oxygen consumption in white adipose tissue (WAT). The mRNA expressions of thermogenesis genes uncoupling protein-1, uncoupling protein-3, carnitine palmitoyltransferase-1 and cell death-inducing DFFA-like effector-a were up-regulated in WAT of the 5X group. Moreover, L. reuteri 263 might induce browning of WAT due to the higher mRNA levels of browning-related genes peroxisome proliferator-activated receptor-γ, PR domain containing-16, Pparγ coactivator-1α, bone morphogenetic protein-7 and fibroblast growth factor-21 in the 1X and 5X groups compared to the HE group. Finally, L. reuteri 263 altered the expressions of genes involved in glucose and lipid metabolisms in WAT, including increasing the levels of glucose transporter type 4 and carbohydrate-responsive element-binding protein and decreasing the expression of Acetyl-CoA carboxylase-1. The results suggest that L. reuteri 263 may treat obesity through energy metabolism remodeling of WAT in the high-energy-diet-induced obese rats.

摘要

肥胖是全球医疗福利的一个严重且代价高昂的问题。益生菌已被提议作为解决肥胖相关问题的候选方案之一,但它们如何对抗肥胖仍未完全了解。在此,我们使用四组 Sprague-Dawley 大鼠(每组 10 只,n=10/group)研究了罗特氏乳杆菌 263(L. reuteri 263)对肥胖的影响,这四组分别为:C(正常饮食,用载体处理)、HE [高能量饮食(HED),用载体处理]、1X(HED 用 2.1×10 CFU/kg/天的 L. reuteri 263 处理)和 5X(HED 用 1.05×10 CFU/kg/天的 L. reuteri 263 处理),持续 8 周。L. reuteri 263 改善了肥胖现象、血清中促炎因子和抗氧化酶的水平。更重要的是,L. reuteri 263 增加了白色脂肪组织(WAT)中的耗氧量。5X 组 WAT 中解偶联蛋白-1、解偶联蛋白-3、肉碱棕榈酰转移酶-1 和细胞死亡诱导 DFFA 样效应因子-a 的生热基因表达上调。此外,由于 1X 和 5X 组的 WAT 中与棕色化相关的基因过氧化物酶体增殖物激活受体-γ、PR 结构域包含蛋白 16、Pparγ 共激活因子 1α、骨形态发生蛋白-7 和成纤维细胞生长因子-21 的 mRNA 水平较高,L. reuteri 263 可能诱导 WAT 棕色化。最后,L. reuteri 263 改变了 WAT 中参与葡萄糖和脂质代谢的基因的表达,包括增加葡萄糖转运蛋白 4 和碳水化合物反应元件结合蛋白的水平,降低乙酰辅酶 A 羧化酶-1 的表达。结果表明,L. reuteri 263 可能通过高能饮食诱导肥胖大鼠 WAT 的能量代谢重塑来治疗肥胖。

相似文献

1
Antiobesity effect of Lactobacillus reuteri 263 associated with energy metabolism remodeling of white adipose tissue in high-energy-diet-fed rats.嗜酸乳杆菌 263 与高能饮食喂养大鼠白色脂肪组织能量代谢重塑相关的抗肥胖作用。
J Nutr Biochem. 2018 Apr;54:87-94. doi: 10.1016/j.jnutbio.2017.11.004. Epub 2017 Nov 16.
2
Green tea extract induces genes related to browning of white adipose tissue and limits weight-gain in high energy diet-fed rat.绿茶提取物可诱导与白色脂肪组织褐变相关的基因,并限制高能饮食喂养大鼠的体重增加。
Food Nutr Res. 2017 Jul 14;61(1):1347480. doi: 10.1080/16546628.2017.1347480. eCollection 2017.
3
Cinnamaldehyde Ameliorates Diet-Induced Obesity in Mice by Inducing Browning of White Adipose Tissue.肉桂醛通过诱导白色脂肪组织褐变改善饮食诱导的小鼠肥胖。
Cell Physiol Biochem. 2017;42(4):1514-1525. doi: 10.1159/000479268. Epub 2017 Jul 18.
4
Lycopene attenuates body weight gain through induction of browning via regulation of peroxisome proliferator-activated receptor γ in high-fat diet-induced obese mice.番茄红素通过调节过氧化物酶体增殖物激活受体 γ 诱导肥胖诱导的棕色化来减轻体重增加。
J Nutr Biochem. 2020 Apr;78:108335. doi: 10.1016/j.jnutbio.2019.108335. Epub 2020 Jan 7.
5
Emodin Improves Glucose and Lipid Metabolism Disorders in Obese Mice Activating Brown Adipose Tissue and Inducing Browning of White Adipose Tissue.大黄素通过激活棕色脂肪组织和诱导白色脂肪组织褐变改善肥胖小鼠的糖脂代谢紊乱。
Front Endocrinol (Lausanne). 2021 May 10;12:618037. doi: 10.3389/fendo.2021.618037. eCollection 2021.
6
Two key temporally distinguishable molecular and cellular components of white adipose tissue browning during cold acclimation.在冷适应过程中,白色脂肪组织褐变存在两个在时间上可区分的关键分子和细胞成分。
J Physiol. 2015 Aug 1;593(15):3267-80. doi: 10.1113/JP270805. Epub 2015 Jul 14.
7
Effect of quercetin on nonshivering thermogenesis of brown adipose tissue in high-fat diet-induced obese mice.槲皮素对高脂饮食诱导肥胖小鼠棕色脂肪组织非颤抖产热的影响。
J Nutr Biochem. 2021 Feb;88:108532. doi: 10.1016/j.jnutbio.2020.108532. Epub 2020 Oct 29.
8
Nutmeg extract potentially alters characteristics of white adipose tissue in rats.肉豆蔻提取物可能改变大鼠白色脂肪组织的特征。
Vet Med Sci. 2021 Mar;7(2):512-520. doi: 10.1002/vms3.383. Epub 2021 Jan 3.
9
Enzymatically synthesized glycogen reduces lipid accumulation in diet-induced obese rats.酶合成的糖原可减少饮食诱导肥胖大鼠的脂肪积累。
Nutr Res. 2013 Sep;33(9):743-52. doi: 10.1016/j.nutres.2013.06.006. Epub 2013 Aug 1.
10
Adiponectin/SIRT1 Axis Induces White Adipose Browning After Vertical Sleeve Gastrectomy of Obese Rats with Type 2 Diabetes.脂联素/SIRT1 轴在 2 型糖尿病肥胖大鼠垂直袖状胃切除术后诱导白色脂肪棕色化。
Obes Surg. 2020 Apr;30(4):1392-1403. doi: 10.1007/s11695-019-04295-4.

引用本文的文献

1
Microbiome, Potential Therapeutic Agents: New Players of Obesity Treatment.微生物群、潜在治疗剂:肥胖治疗的新参与者
J Microbiol Biotechnol. 2025 Apr 24;35:e2501024. doi: 10.4014/jmb.2501.01024.
2
The Impact of on Oral and Systemic Health: A Comprehensive Review of Recent Research.关于[具体内容缺失]对口腔和全身健康的影响:近期研究的综合综述。
Microorganisms. 2024 Dec 30;13(1):45. doi: 10.3390/microorganisms13010045.
3
Lactobacillus reuteri ZJ617 attenuates metabolic syndrome via microbiota-derived spermidine.罗伊氏乳杆菌ZJ617通过微生物群衍生的亚精胺减轻代谢综合征。
Nat Commun. 2025 Jan 21;16(1):877. doi: 10.1038/s41467-025-56105-4.
4
L11 and LR: Ameliorate Obesity via AMPK Pathway.L11和LR:通过AMPK途径改善肥胖。
Nutrients. 2024 Dec 24;17(1):4. doi: 10.3390/nu17010004.
5
The association between gut microbiota and resting metabolic rate in overweight/obese women: a case-control study.超重/肥胖女性肠道微生物群与静息代谢率之间的关联:一项病例对照研究。
J Diabetes Metab Disord. 2023 Dec 30;23(1):931-941. doi: 10.1007/s40200-023-01368-1. eCollection 2024 Jun.
6
Postbiotic potential of KMU01 cell-free supernatant for the alleviation of obesity in mice.KMU01无细胞上清液对减轻小鼠肥胖的后生元潜力。
Heliyon. 2024 Feb 7;10(5):e25263. doi: 10.1016/j.heliyon.2024.e25263. eCollection 2024 Mar 15.
7
Cheese containing probiotic NJ42 isolated from stingless bee honey reduces weight gain, fat accumulation, and glucose intolerance in mice.含有从无刺蜂蜂蜜中分离出的益生菌NJ42的奶酪可减轻小鼠的体重增加、脂肪堆积和葡萄糖不耐受。
Heliyon. 2024 Feb 10;10(4):e25981. doi: 10.1016/j.heliyon.2024.e25981. eCollection 2024 Feb 29.
8
Obese Ningxiang pig-derived microbiota rewires carnitine metabolism to promote muscle fatty acid deposition in lean DLY pigs.肥胖宁乡猪源微生物群重塑肉碱代谢以促进瘦肉型杜洛克×长白猪×大白猪杂交猪肌肉脂肪酸沉积。
Innovation (Camb). 2023 Jul 26;4(5):100486. doi: 10.1016/j.xinn.2023.100486. eCollection 2023 Sep 11.
9
Interplay of Gut Microbiota in Polycystic Ovarian Syndrome: Role of Gut Microbiota, Mechanistic Pathways and Potential Treatment Strategies.肠道微生物群在多囊卵巢综合征中的相互作用:肠道微生物群的作用、作用机制途径及潜在治疗策略
Pharmaceuticals (Basel). 2023 Jan 28;16(2):197. doi: 10.3390/ph16020197.
10
Probiotic Limosilactobacillus Reuteri (Lactobacillus Reuteri) Extends the Lifespan of Drosophila Melanogaster through Insulin/IGF-1 Signaling.益生菌路氏乳杆菌(罗伊氏乳杆菌)通过胰岛素/胰岛素样生长因子-1信号通路延长黑腹果蝇的寿命。
Aging Dis. 2023 Aug 1;14(4):1407-1424. doi: 10.14336/AD.2023.0122.