Abstract
Obesity is a complex and heterogeneous condition resulting from multiple genetic and environmental factors each interacting in a variety of ways. For example, obesity can develop as a consequence of adversely regulated metabolic pathways (e.g., catecholaminergic pathways, leptin signaling pathways, insulin signaling pathways, lipid oxidation pathways), each being potentially influenced by a number of genetic determinants. Furthermore, the expression of genetic propensities may depend on synergistic relationships among genes (epistasis), exposure to certain environmental stimuli (gene-by-environment interactions) such as nutritional or activity backgrounds, developmental stage, epigenetic events, or sex of the individual. Given the multiplicity of factors underlying the predisposition to obesity, complex modeling approaches such as those used in genetic epidemiology have been used to uncover genetic and environmental factors, to explore how those factors act and interact, and to estimate the magnitudes of those effects. Based on designs that depend on predictable underlying biological relationships (e.g., degree of relatedness between family members), these models provide inferences about genes. They do not depend on direct measures of the genes, but they rather infer genetic effects based on biological modeling.
| Original language | English |
|---|---|
| Title of host publication | Handbook of Obesity |
| Subtitle of host publication | Epidemiology, Etiology, and Physiopathology, Third Edition |
| Publisher | CRC Press |
| Pages | 91-104 |
| Number of pages | 14 |
| ISBN (Electronic) | 9781842145579 |
| ISBN (Print) | 9781842145562 |
| State | Published - Jan 1 2014 |