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Abstract

Obesity results when food intake exceeds energy expenditure. It is a complex multifactoral disease that appears to involve the interaction of numerous neuronal circuits. The current theory states that phenotypic expression of obesity depends on the influence of environmental factors upon an underlying pool of genes that determine susceptibility. However, the nature of this inherited predisposition remains unclear. Recent years have witnessed considerable progress in our understanding. Rodents continue to be central to this study, providing ideal models to determine the means by which the various regulatory pathways interact in different feeding states. In particular, observations from the dietary-induced obese state have yielded valuable information regarding the identity of candidate susceptibility genes. Mutations within some of the lead players identified have since been discovered in obese humans. Such information is a prerequisite for successful treatment of the disorder and the curbing of further increases in body weight across future generations.

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Harrold, J. (2001). Genetic Susceptibility of Rodents to Diet-Induced Obesity. In: Owen, J.B., Treasure, J.L., Collier, D.A. (eds) Animal Models — Disorders of Eating Behaviour and Body Composition. Springer, Dordrecht. https://doi.org/10.1007/978-94-015-9662-6_8

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  • DOI: https://doi.org/10.1007/978-94-015-9662-6_8

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