• 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

白色脂肪组织的褐变:一些燃烧的问题。

The browning of white adipose tissue: some burning issues.

机构信息

Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 106 91 Stockholm, Sweden.

Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 106 91 Stockholm, Sweden.

出版信息

Cell Metab. 2014 Sep 2;20(3):396-407. doi: 10.1016/j.cmet.2014.07.005. Epub 2014 Aug 7.

DOI:10.1016/j.cmet.2014.07.005
PMID:25127354
Abstract

Igniting thermogenesis within white adipose tissue (i.e., promoting expression and activity of the uncoupling protein UCP1) has attracted much interest. Numerous "browning agents" have now been described (gene ablations, transgenes, food components, drugs, environments, etc.). The implied action of browning agents is that they increase UCP1 through this heat production, leading to slimming. Here, we particularly point to the possibility that cause and effect may on occasion be the reverse: browning agents may disrupt, for example, the fur, leading to increased heat loss, increased thermogenic demand to counteract this heat loss, and thus, through sympathetic nervous system activation, to enhanced UCP1 expression in white (and brown) adipose tissues.

摘要

在内皮脂肪组织中引发产热(即促进解偶联蛋白 UCP1 的表达和活性)引起了广泛关注。现在已经描述了许多“褐色化剂”(基因缺失、转基因、食物成分、药物、环境等)。褐色化剂的作用是通过这种产热增加 UCP1,从而导致减肥。在这里,我们特别指出,有时因果关系可能相反:褐色化剂可能会破坏皮毛,导致热量损失增加,为了抵消这种热量损失,会增加产热需求,从而通过交感神经系统的激活,增强白色(和棕色)脂肪组织中 UCP1 的表达。

相似文献

1
The browning of white adipose tissue: some burning issues.白色脂肪组织的褐变:一些燃烧的问题。
Cell Metab. 2014 Sep 2;20(3):396-407. doi: 10.1016/j.cmet.2014.07.005. Epub 2014 Aug 7.
2
UCP1 in brite/beige adipose tissue mitochondria is functionally thermogenic.米色脂肪组织线粒体中的解偶联蛋白1具有产热功能。
Cell Rep. 2013 Dec 12;5(5):1196-203. doi: 10.1016/j.celrep.2013.10.044. Epub 2013 Nov 27.
3
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.
4
Cold-inducible Zfp516 activates UCP1 transcription to promote browning of white fat and development of brown fat.冷诱导的Zfp516激活UCP1转录以促进白色脂肪棕色化和棕色脂肪发育。
Mol Cell. 2015 Jan 22;57(2):235-46. doi: 10.1016/j.molcel.2014.12.005. Epub 2015 Jan 8.
5
Central Fibroblast Growth Factor 21 Browns White Fat via Sympathetic Action in Male Mice.中枢成纤维细胞生长因子21通过交感神经作用使雄性小鼠白色脂肪褐色化
Endocrinology. 2015 Jul;156(7):2470-81. doi: 10.1210/en.2014-2001. Epub 2015 Apr 29.
6
Dietary factors evoke thermogenesis in adipose tissues.饮食因素可引起脂肪组织产热。
Obes Res Clin Pract. 2014 Nov-Dec;8(6):e533-9. doi: 10.1016/j.orcp.2013.12.002. Epub 2014 Jan 18.
7
Pharmacologic Effects of FGF21 Are Independent of the "Browning" of White Adipose Tissue.FGF21 的药理作用不依赖于白色脂肪组织的“褐色化”。
Cell Metab. 2015 May 5;21(5):731-8. doi: 10.1016/j.cmet.2015.04.019.
8
Breaking BAT: can browning create a better white?打破棕色脂肪:棕色化能否塑造更好的白色脂肪?
J Endocrinol. 2016 Jan;228(1):R19-29. doi: 10.1530/JOE-15-0408. Epub 2015 Oct 8.
9
A nutritional perspective on UCP1-dependent thermogenesis.关于解偶联蛋白1(UCP1)依赖性产热的营养视角。
Biochimie. 2017 Mar;134:99-117. doi: 10.1016/j.biochi.2016.12.014. Epub 2017 Jan 3.
10
Metabolic consequences of the presence or absence of the thermogenic capacity of brown adipose tissue in mice (and probably in humans).棕色脂肪组织产热能力存在或缺失对小鼠(可能还有人类)代谢的影响。
Int J Obes (Lond). 2010 Oct;34 Suppl 1:S7-16. doi: 10.1038/ijo.2010.177.

引用本文的文献

1
Navigating the Strengths and Constraints of Mouse Models in Obesity Research.探索肥胖研究中小鼠模型的优势与局限
Endocrinology. 2025 Jul 8;166(9). doi: 10.1210/endocr/bqaf123.
2
analysis of promoters predicts conserved and human specific regulators of adipocyte thermogenesis.启动子分析预测脂肪细胞产热的保守及人类特异性调节因子。
iScience. 2025 Jun 21;28(7):112969. doi: 10.1016/j.isci.2025.112969. eCollection 2025 Jul 18.
3
The Regulator of G Protein Signaling 14 Knockout Mouse, a Model of Healthful Longevity Protects Against Obesity and Glucose Intolerance Through a Brown Adipose Tissue Mechanism.
G蛋白信号调节因子14基因敲除小鼠是健康长寿的模型,通过棕色脂肪组织机制预防肥胖和葡萄糖不耐受。
Int J Mol Sci. 2025 Apr 26;26(9):4113. doi: 10.3390/ijms26094113.
4
Caloric Restriction and Telomere Preservation in TERT Knockout Adipocyte Progenitors Does Not Rescue Mice From Metabolic Dysfunction due to a TERT Function in Adipocyte Mitochondria.热量限制与端粒酶逆转录酶(TERT)基因敲除脂肪细胞祖细胞中端粒的保存无法使小鼠免于因脂肪细胞线粒体中的TERT功能而导致的代谢功能障碍。
Aging Cell. 2025 Mar;24(3):e14499. doi: 10.1111/acel.14499. Epub 2025 Feb 11.
5
TGF-β antagonism synergizes with PPARγ agonism to reduce fibrosis and enhance beige adipogenesis.转化生长因子-β(TGF-β)拮抗作用与过氧化物酶体增殖物激活受体γ(PPARγ)激动作用协同,以减少纤维化并增强米色脂肪生成。
Mol Metab. 2024 Dec;90:102054. doi: 10.1016/j.molmet.2024.102054. Epub 2024 Oct 24.
6
Keys to the switch of fat burning: stimuli that trigger the uncoupling protein 1 (UCP1) activation in adipose tissue.燃烧脂肪的关键:刺激脂肪组织中解偶联蛋白 1(UCP1)的激活。
Lipids Health Dis. 2024 Sep 28;23(1):322. doi: 10.1186/s12944-024-02300-z.
7
Mitophagy Responds to the Environmental Temperature and Regulates Mitochondrial Mass in Adipose Tissues.自噬响应环境温度并调节脂肪组织中线粒体的质量。
Adv Exp Med Biol. 2024;1461:229-243. doi: 10.1007/978-981-97-4584-5_16.
8
The Therapeutic Potential of Theobromine in Obesity: A Comprehensive Review.可可碱在肥胖症中的治疗潜力:全面综述。
Nutr Rev. 2025 May 1;83(5):859-868. doi: 10.1093/nutrit/nuae122.
9
βAR-mTOR-lipin1 pathway mediates PKA-RIIβ deficiency-induced adipose browning.βAR-mTOR-lipin1 通路介导 PKA-RIIβ 缺乏诱导的脂肪棕色化。
Theranostics. 2024 Aug 26;14(13):5316-5335. doi: 10.7150/thno.97046. eCollection 2024.
10
Mechanisms and metabolic consequences of adipocyte progenitor replicative senescence.脂肪细胞祖细胞复制性衰老的机制及代谢后果。
Immunometabolism (Cobham). 2024 Aug 28;6(3):e00046. doi: 10.1097/IN9.0000000000000046. eCollection 2024 Jul.