Abstractions
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 in | Nature (London) Vol. 452; no. 7186; p. xiii |
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Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
27.03.2008
Nature Publishing Group |
Subjects | |
Online Access | Get full text |
ISSN | 0028-0836 1476-4687 |
DOI | 10.1038/7186xiiib |
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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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Bibliography: | SourceType-Scholarly Journals-1 content type line 14 ObjectType-Interview-1 |
ISSN: | 0028-0836 1476-4687 |
DOI: | 10.1038/7186xiiib |