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Uncoupling proteins mRNA levels in mice lacking acylation-stimulating protein

The etiology of obesity involves imbalanced energy intake and utilization. ASP is an adipose tissue hormone that facilitates adipocyte uptake of serum fatty acids and their storage. Mice lacking ASP have less adipose tissue mass, despite increased food intake, than wild-type littermates. We hypothesize that the unstored fuels are oxidized through UCP (thermogenic mitochondrial carriers). / In male ASP-deficient mice mRNA levels were measured by semi-quantitative RT-PCR and the following changes were observed: UCP-1 decreased in all tested tissues, UCP-2 increased by 15% and 6 fold in muscle and white adipose tissue and UCP-3 increased 2.5 and 10 fold in muscle and epididymal adipose tissue, respectively. In female ASP-deficient mice UCP-1 decreased in all tissues, UCP-2 increased by 10% and 40% in inguinal and brown adipose tissue, respectively, and UCP-3 remained stable in all tissues. High fat diet nullified these differences, and decreased all wild-type UCP levels. / We propose that UCP-2 and 3 assume the role of UCP-1 in fuel utilization, thus helping mice face an increased energy load in the absence of ASP.

Identiferoai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.33018
Date January 2001
CreatorsSimion, Oana-Maria.
ContributorsCianflone, Katherine (advisor)
PublisherMcGill University
Source SetsLibrary and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada
LanguageEnglish
Detected LanguageEnglish
TypeElectronic Thesis or Dissertation
Formatapplication/pdf
CoverageMaster of Science (Division of Experimental Medicine.)
RightsAll items in eScholarship@McGill are protected by copyright with all rights reserved unless otherwise indicated.
Relationalephsysno: 001838276, proquestno: MQ75332, Theses scanned by UMI/ProQuest.

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