دورية أكاديمية
أعرض في EDS

ThermoMouse: an in vivo model to identify modulators of UCP1 expression in brown adipose tissue.

التفاصيل البيبلوغرافية
العنوان: ThermoMouse: an in vivo model to identify modulators of UCP1 expression in brown adipose tissue.
المؤلفون: Galmozzi A; Department of Chemical Physiology and The Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, CA 92037, USA., Sonne SB; UCSF Diabetes Center, Department of Cell and Tissue Biology, University of California, San Francisco, 35 Medical Center Way, San Francisco, CA 94143, USA., Altshuler-Keylin S; UCSF Diabetes Center, Department of Cell and Tissue Biology, University of California, San Francisco, 35 Medical Center Way, San Francisco, CA 94143, USA., Hasegawa Y; UCSF Diabetes Center, Department of Cell and Tissue Biology, University of California, San Francisco, 35 Medical Center Way, San Francisco, CA 94143, USA., Shinoda K; UCSF Diabetes Center, Department of Cell and Tissue Biology, University of California, San Francisco, 35 Medical Center Way, San Francisco, CA 94143, USA., Luijten IHN; UCSF Diabetes Center, Department of Cell and Tissue Biology, University of California, San Francisco, 35 Medical Center Way, San Francisco, CA 94143, USA., Chang JW; Department of Chemical Physiology and The Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, CA 92037, USA., Sharp LZ; UCSF Diabetes Center, Department of Cell and Tissue Biology, University of California, San Francisco, 35 Medical Center Way, San Francisco, CA 94143, USA., Cravatt BF; Department of Chemical Physiology and The Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, CA 92037, USA., Saez E; Department of Chemical Physiology and The Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, CA 92037, USA. Electronic address: esaez@scripps.edu., Kajimura S; UCSF Diabetes Center, Department of Cell and Tissue Biology, University of California, San Francisco, 35 Medical Center Way, San Francisco, CA 94143, USA. Electronic address: skajimura@diabetes.ucsf.edu.
المصدر: Cell reports [Cell Rep] 2014 Dec 11; Vol. 9 (5), pp. 1584-1593. Date of Electronic Publication: 2014 Nov 26.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: United States NLM ID: 101573691 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2211-1247 (Electronic) NLM ISO Abbreviation: Cell Rep Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [Cambridge, MA] : Cell Press, c 2012-
مواضيع طبية MeSH: Adipose Tissue, Brown/*metabolism , Ion Channels/*metabolism , Mitochondrial Proteins/*metabolism , Transcriptional Activation/*drug effects, Animals ; Anti-Obesity Agents/pharmacology ; Cells, Cultured ; Drug Evaluation, Preclinical ; Energy Metabolism ; Gene Expression ; Ion Channels/genetics ; Male ; Mice, Transgenic ; Mitochondrial Proteins/genetics ; Obesity/drug therapy ; Obesity/metabolism ; Signal Transduction ; Thermogenesis ; Uncoupling Protein 1
مستخلص: Obesity develops when energy intake chronically exceeds energy expenditure. Because brown adipose tissue (BAT) dissipates energy in the form of heat, increasing energy expenditure by augmenting BAT-mediated thermogenesis may represent an approach to counter obesity and its complications. The ability of BAT to dissipate energy is dependent on expression of mitochondrial uncoupling protein 1 (UCP1). To facilitate the identification of pharmacological modulators of BAT UCP1 levels, which may have potential as antiobesity medications, we developed a transgenic model in which luciferase activity faithfully mimics endogenous UCP1 expression and its response to physiologic stimuli. Phenotypic screening of a library using cells derived from this model yielded a small molecule that increases UCP1 expression in brown fat cells and mice. Upon adrenergic stimulation, compound-treated mice showed increased energy expenditure. These tools offer an opportunity to identify pharmacologic modulators of UCP1 expression and uncover regulatory pathways that impact BAT-mediated thermogenesis.
(Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.)
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معلومات مُعتمدة: P30 DK063720 United States DK NIDDK NIH HHS; DK63720 United States DK NIDDK NIH HHS; R01 DK097441 United States DK NIDDK NIH HHS; T32 DK007418 United States DK NIDDK NIH HHS; DK087853 United States DK NIDDK NIH HHS; K99 DK087853 United States DK NIDDK NIH HHS; CA179489 United States CA NCI NIH HHS; DK099810 United States DK NIDDK NIH HHS; DK97441 United States DK NIDDK NIH HHS; S10 OD016357 United States OD NIH HHS; R21 CA179489 United States CA NCI NIH HHS; R24 DK099810 United States DK NIDDK NIH HHS; T32 HD007470 United States HD NICHD NIH HHS; R00 DK087853 United States DK NIDDK NIH HHS
المشرفين على المادة: 0 (Anti-Obesity Agents)
0 (Ion Channels)
0 (Mitochondrial Proteins)
0 (Ucp1 protein, mouse)
0 (Uncoupling Protein 1)
تواريخ الأحداث: Date Created: 20141204 Date Completed: 20150817 Latest Revision: 20220316
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC4268417
DOI: 10.1016/j.celrep.2014.10.066
PMID: 25466254
قاعدة البيانات: MEDLINE
الوصف
تدمد:2211-1247
DOI:10.1016/j.celrep.2014.10.066