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<pubDate>Sun, 27 Jul 2008 07:31:05 BST</pubDate>


	<title>CiteULike: omalbam's library [235 articles]</title>
	<description>CiteULike: omalbam's library [235 articles]</description>


	<link>http://www.citeulike.org/user/omalbam/article/2697905</link>
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    <title>Variations in the uncoupling protein-3 gene are associated with specific obesity phenotypes</title>
    <link>http://www.citeulike.org/user/omalbam/article/2697905</link>
    <description>&lt;i&gt;Eur J Endocrinol, Vol. 158, No. 5. (1 May 2008), pp. 669-676.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;ObjectiveUncoupling protein 3 (UCP-3) uncouples oxidative metabolism from ATP synthesis, resulting in the production of heat instead of energy storage. Single nucleotide polymorphisms (SNPs) in UCP-3 might result in a reduced function or expression of UCP-3 and therefore lead to an increased capacity to store energy as fat. DesignWe conducted a population-based, cross-sectional single-center study among 400 Dutch men between 40 and 80 years. MethodsSeven SNPs in the UCP-3 gene were genotyped by means of an allele-specific real-time TaqMan PCR. Linear regression analyses were performed to examine the independent effects of these SNPs on obesity phenotypes. ResultsWe found a significant association between homozygosity for the minor allele of rs647126, rs1685356, and rs2075577 and an increase in body mass index (BMI; P=0.033, P=0.016, and P=0.019 respectively). Heterozygosity for rs1685354 was associated with a significant decrease in visceral fat mass (P=0.030). ConclusionsOur results suggest that genetic variations in the UCP-3 gene are associated with an increase in BMI. A plausible mechanism by which these SNPs lead to an increase in BMI is that due to these SNPs, the UCP-3 activity might be decreased. As a result, uncoupling activity may also decrease, which will lead to an increase in body weight and BMI. 10.1530/EJE-07-0834</description>
    <dc:title>Variations in the uncoupling protein-3 gene are associated with specific obesity phenotypes</dc:title>

    <dc:creator>Annet van Abeelen</dc:creator>
    <dc:creator>Mariken de Krom</dc:creator>
    <dc:creator>Judith Hendriks</dc:creator>
    <dc:creator>Diederick Grobbee</dc:creator>
    <dc:creator>Roger Adan</dc:creator>
    <dc:creator>Yvonne van der Schouw</dc:creator>
    <dc:identifier>doi:10.1530/EJE-07-0834</dc:identifier>
    <dc:source>Eur J Endocrinol, Vol. 158, No. 5. (1 May 2008), pp. 669-676.</dc:source>
    <dc:date>2008-04-21T19:09:45-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Eur J Endocrinol</prism:publicationName>
    <prism:volume>158</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>669</prism:startingPage>
    <prism:endingPage>676</prism:endingPage>
    <prism:category>diagnosis</prism:category>
    <prism:category>molecular</prism:category>
    <prism:category>obesity</prism:category>
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