• 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

肥胖动物模型概述

Overview of animal models of obesity.

作者信息

Lutz Thomas A, Woods Stephen C

机构信息

University of Zurich, Institute of Veterinary Physiology, Zurich Center of Integrative Human Physiology, Zurich, Switzerland.

出版信息

Curr Protoc Pharmacol. 2012 Sep;Chapter 5:Unit5.61. doi: 10.1002/0471141755.ph0561s58.

DOI:10.1002/0471141755.ph0561s58
PMID:22948848
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3482633/
Abstract

The focus of this overview is on the animal models of obesity most commonly utilized in research. The models include monogenic models in the leptin pathway, polygenic diet-dependent models, and, in particular for their historical perspective, surgical and chemical models of obesity. However, there are far too many models to consider all of them comprehensively, especially those caused by selective molecular genetic approaches modifying one or more genes in specific populations of cells. Further, the generation and use of inducible transgenic animals (induced knock-out or knock-in) is not covered, even though they often carry significant advantages compared to traditional transgenic animals, e.g., influences of the genetic modification during the development of the animals can be minimized. The number of these animal models is simply too large to be covered in this unit.

摘要

本综述的重点是研究中最常用的肥胖动物模型。这些模型包括瘦素途径中的单基因模型、多基因饮食依赖模型,特别是从历史角度来看的肥胖手术和化学模型。然而,模型数量太多,无法全面考虑所有模型,尤其是那些通过选择性分子遗传学方法在特定细胞群体中修饰一个或多个基因而导致的模型。此外,本单元不涉及诱导型转基因动物(诱导敲除或敲入)的产生和使用,尽管与传统转基因动物相比,它们通常具有显著优势,例如,可以将动物发育过程中基因修饰的影响降至最低。这些动物模型的数量实在太多,无法在本单元中涵盖。

相似文献

1
Overview of animal models of obesity.肥胖动物模型概述
Curr Protoc Pharmacol. 2012 Sep;Chapter 5:Unit5.61. doi: 10.1002/0471141755.ph0561s58.
2
Lentiviral vector-mediated knockdown of Lrb in the arcuate nucleus promotes diet-induced obesity in rats.慢病毒载体介导的弓状核中 Lrb 的敲低可促进大鼠饮食诱导的肥胖。
J Mol Endocrinol. 2013 May 17;51(1):27-35. doi: 10.1530/JME-12-0212. Print 2013.
3
Deletion of Suppressor of Cytokine Signaling 3 from Forebrain Neurons Delays Infertility and Onset of Hypothalamic Leptin Resistance in Response to a High Caloric Diet.从前脑神经元中删除细胞因子信号转导抑制因子3可延缓高热量饮食导致的不育和下丘脑瘦素抵抗的发生。
J Neurosci. 2016 Jul 6;36(27):7142-53. doi: 10.1523/JNEUROSCI.2714-14.2016.
4
Single-Nucleus RNA Sequencing of the Hypothalamic Arcuate Nucleus of C57BL/6J Mice After Prolonged Diet-Induced Obesity.延长饮食诱导肥胖后 C57BL/6J 小鼠下丘脑弓状核的单细胞 RNA 测序。
Hypertension. 2020 Aug;76(2):589-597. doi: 10.1161/HYPERTENSIONAHA.120.15137. Epub 2020 Jun 8.
5
A spontaneous leptin receptor point mutation causes obesity and differentially affects leptin signaling in hypothalamic nuclei resulting in metabolic dysfunctions distinct from db/db mice.一种自发性瘦素受体点突变导致肥胖,并在不同程度上影响下丘脑核内的瘦素信号,导致与 db/db 小鼠不同的代谢功能障碍。
Mol Metab. 2019 Jul;25:131-141. doi: 10.1016/j.molmet.2019.04.010. Epub 2019 Apr 25.
6
Downregulation of leptin receptor and kisspeptin/GPR54 in the murine hypothalamus contributes to male hypogonadism caused by high-fat diet-induced obesity.瘦素受体和 kisspeptin/GPR54 在肥胖型高脂肪饮食诱导的雄性性腺功能减退症小鼠下丘脑的下调。
Endocrine. 2018 Oct;62(1):195-206. doi: 10.1007/s12020-018-1646-9. Epub 2018 Jun 13.
7
An Overview of Rodent Models of Obesity and Type 2 Diabetes.肥胖症和 2 型糖尿病啮齿动物模型概述。
Methods Mol Biol. 2020;2128:11-24. doi: 10.1007/978-1-0716-0385-7_2.
8
Pro-opiomelanocortin gene transfer to the nucleus of the solitary track but not arcuate nucleus ameliorates chronic diet-induced obesity.促阿黑皮素原基因转染孤束核而非弓状核可改善慢性饮食诱导的肥胖。
Neuroscience. 2010 Sep 15;169(4):1662-71. doi: 10.1016/j.neuroscience.2010.06.001. Epub 2010 Jun 9.
9
Deletion of the serotonin 2c receptor from transgenic mice overexpressing leptin does not affect their lipodystrophy but exacerbates their diet-induced obesity.从过表达瘦素的转基因小鼠中删除血清素2c受体不会影响它们的脂肪营养不良,但会加剧它们因饮食引起的肥胖。
Biochem Biophys Res Commun. 2006 Dec 15;351(2):418-23. doi: 10.1016/j.bbrc.2006.10.033. Epub 2006 Oct 24.
10
Cafeteria diet-induced obesity reduces leptin-stimulated NADPH-diaphorase reactivity in the hypothalamic arcuate nucleus of rats. cafeteria 饮食诱导的肥胖会降低大鼠下丘脑弓状核中瘦素刺激的 NADPH 黄递酶反应性。
Acta Histochem. 2020 Oct;122(7):151616. doi: 10.1016/j.acthis.2020.151616. Epub 2020 Aug 24.

引用本文的文献

1
Exploring molecular links between obesity and osteoporosis: insights from in-silico analysis and mannose supplementation.探索肥胖与骨质疏松症之间的分子联系:来自计算机模拟分析和甘露糖补充的见解。
Sci Rep. 2025 Aug 11;15(1):29384. doi: 10.1038/s41598-025-07294-x.
2
The obesity paradox in murine sepsis models: a systematic review and meta-analysis.小鼠脓毒症模型中的肥胖悖论:一项系统综述和荟萃分析。
Anaesthesiol Intensive Ther. 2025 Jul 25;57(1):182-194. doi: 10.5114/ait/207612.
3
Murine Models of Obesity-Related Cancer Risk.肥胖相关癌症风险的小鼠模型
Cancer Prev Res (Phila). 2025 Jun 13. doi: 10.1158/1940-6207.CAPR-24-0545.
4
From Genes to Environment: Elucidating Pancreatic Carcinogenesis Through Genetically Engineered and Risk Factor-Integrated Mouse Models.从基因到环境:通过基因工程和风险因素整合小鼠模型阐明胰腺癌发生机制
Cancers (Basel). 2025 May 15;17(10):1676. doi: 10.3390/cancers17101676.
5
Sexual dimorphism in animal models of heart failure with preserved ejection fraction.射血分数保留的心力衰竭动物模型中的性别二态性。
J Appl Physiol (1985). 2025 Jun 1;138(6):1449-1473. doi: 10.1152/japplphysiol.00595.2024. Epub 2025 May 5.
6
Epigenetic Mechanisms of Obesity: Insights from Transgenic Animal Models.肥胖的表观遗传机制:来自转基因动物模型的见解
Life (Basel). 2025 Apr 16;15(4):653. doi: 10.3390/life15040653.
7
Coactosin-like F-actin binding protein (Cotl1) plays a key role in adipocyte differentiation and obesity.类肌动蛋白结合蛋白(Cotl1)在脂肪细胞分化和肥胖中起关键作用。
Commun Biol. 2025 Apr 17;8(1):628. doi: 10.1038/s42003-025-08062-3.
8
Transcriptome-guided GLP-1 receptor therapy rescues metabolic and behavioral disruptions in a Bardet-Biedl syndrome mouse model.转录组引导的胰高血糖素样肽-1受体疗法挽救了巴德-比德尔综合征小鼠模型中的代谢和行为紊乱。
J Clin Invest. 2025 Apr 15;135(12). doi: 10.1172/JCI184636. eCollection 2025 Jun 16.
9
Phosphorylation of an RNA-Binding Protein Rck/Me31b by Hippo Is Essential for Adipose Tissue Aging.Hippo对RNA结合蛋白Rck/Me31b的磷酸化作用对脂肪组织衰老至关重要。
Aging Cell. 2025 Jun;24(6):e70022. doi: 10.1111/acel.70022. Epub 2025 Mar 11.
10
The Interplay of Genetic Predisposition, Circadian Misalignment, and Metabolic Regulation in Obesity.遗传易感性、昼夜节律失调与肥胖中代谢调节的相互作用
Curr Obes Rep. 2025 Mar 1;14(1):21. doi: 10.1007/s13679-025-00613-3.

本文引用的文献

1
The regulation of food intake in mammalian hibernators: a review.哺乳动物冬眠者摄食调节的研究进展综述。
J Comp Physiol B. 2012 May;182(4):451-67. doi: 10.1007/s00360-011-0630-y. Epub 2011 Nov 12.
2
Ovariectomy and overeating palatable, energy-dense food increase subcutaneous adipose tissue more than intra-abdominal adipose tissue in rats.卵巢切除术和暴食可口、高热量食物会使大鼠的皮下脂肪组织比腹腔内脂肪组织增加更多。
Biol Sex Differ. 2011 May 11;2:6. doi: 10.1186/2042-6410-2-6.
3
Melanocortin receptor 4 deficiency affects body weight regulation, grooming behavior, and substrate preference in the rat.黑素皮质素受体 4 缺乏影响大鼠的体重调节、梳理行为和底物偏好。
Obesity (Silver Spring). 2012 Mar;20(3):612-21. doi: 10.1038/oby.2011.81. Epub 2011 Apr 28.
4
Dietary manipulation reveals an unexpected inverse relationship between fat mass and adipose 11β-hydroxysteroid dehydrogenase type 1.饮食干预揭示了脂肪质量与脂肪组织 11β-羟类固醇脱氢酶 1 之间出人意料的反比关系。
Am J Physiol Endocrinol Metab. 2011 Jun;300(6):E1076-84. doi: 10.1152/ajpendo.00531.2010. Epub 2011 Mar 15.
5
Loss of agouti-related peptide does not significantly impact the phenotype of murine POMC deficiency.缺失 agouti 相关肽对小鼠 POMC 缺乏表型的影响不显著。
Endocrinology. 2011 May;152(5):1819-28. doi: 10.1210/en.2010-1450. Epub 2011 Mar 1.
6
Consumption of a high-fat diet induces central insulin resistance independent of adiposity.高脂肪饮食摄入会导致中枢性胰岛素抵抗,与肥胖无关。
Physiol Behav. 2011 Apr 18;103(1):10-6. doi: 10.1016/j.physbeh.2011.01.010. Epub 2011 Jan 15.
7
Toward a more complete (and less controversial) understanding of energy expenditure and its role in obesity pathogenesis.朝着对能量消耗及其在肥胖发病机制中的作用有更全面(且争议较小)的理解。
Diabetes. 2011 Jan;60(1):17-23. doi: 10.2337/db10-0909.
8
Perinatal exposure to high-fat diet programs energy balance, metabolism and behavior in adulthood.围产期高脂肪饮食可引起成年后能量平衡、代谢和行为的改变。
Neuroendocrinology. 2011;93(1):1-8. doi: 10.1159/000322038. Epub 2010 Nov 13.
9
High-fat diet-induced obesity in animal models.高脂肪饮食诱导的动物模型肥胖。
Nutr Res Rev. 2010 Dec;23(2):270-99. doi: 10.1017/S0954422410000168. Epub 2010 Oct 27.
10
Lipodystrophy: metabolic insights from a rare disorder.脂肪代谢障碍:罕见疾病带来的代谢新见解。
J Endocrinol. 2010 Dec;207(3):245-55. doi: 10.1677/JOE-10-0272. Epub 2010 Sep 24.