Obesity susceptibility and genetics, a complex

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 andPpm1l— 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.
This is such interesting work. There must be a range of disease liabilities from the direct relationship of gene change and Haemophilia or Thalassaemia to the consequences of a complex web of interconnecting genes and an accumulated liability prompted by the environment being conducive to such developing obesity and atheroma.
Emilsson et al 2008, Genetics of gene expression and its effect on disease Nature vol 453 pp 423-428
Chen et al 2008, Variations in DNA elucidation molecular networks that cause disease. Nature vol 452 pp 429-435

Martin Eastwood
Back to top