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Obesity gets complicated Complex human diseases result from the interplay of many genetic and environmental factors. To build up a picture of the factors contributing to one such disease, obesity, gene expression was evaluated as a quantitative trait in blood and adipose tissue samples from hundreds...

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Published inNature (London) Vol. 452; no. 7186; p. xiii
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 27.03.2008
Nature Publishing Group
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ISSN0028-0836
1476-4687
DOI10.1038/7186xiiib

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Summary:Obesity gets complicated Complex human diseases result from the interplay of many genetic and environmental factors. To build up a picture of the factors contributing to one such disease, obesity, gene expression was evaluated as a quantitative trait in blood and adipose tissue samples from hundreds of Icelandic subjects aged 18 to 85. The results reveal a tendency to certain characteristic patterns of gene activation in the fatty tissues — though to a much lesser extent in the blood — of people with a higher body mass index. A transcriptional network constructed from the adipose tissue data has significant overlap with a network based on mouse adipose tissue data. Experimental support for the idea that complex diseases are emergent properties of molecular networks influenced by genes and environment comes from a study in mice. Mice were examined for disturbances in genetic expression networks that correlate with metabolic traits associated with obesity, diabetes and atherosclerosis. Three genes — Lpl , Lactb and Ppm1l — were identified as previously unknown obesity genes. This 'molecular network' approach raises the prospect that therapies might be directed at whole 'disease networks', rather than at one or two specific genes.
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ISSN:0028-0836
1476-4687
DOI:10.1038/7186xiiib