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Review
. 2006 Aug;53(4):777-94.
doi: 10.1016/j.pcl.2006.05.011.

Obesity and its therapy: from genes to community action

Joseph A Skelton  1 , Laure DeMattia, Lawrence Miller, Michael Olivier
Affiliations
Review

Obesity and its therapy: from genes to community action

Joseph A Skelton et al. Pediatr Clin North Am. 2006 Aug.

Abstract

Like many diseases, the causes of obesity are complex, and their investigation requires novel approaches. Given the many contributors to our weight status, as well as the dynamic nature, genomic tools must be applied in an ecological model. Evaluating disparate factors can be difficult, such as feeding behavior, nutritional genomics, and gene-environment interaction. Many of these behaviors are being evaluated in animal models and hold great promise for targeted interventions in the future.

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Figures

Fig. 1
Fig. 1
Biopsychosocial model of obesity.
Fig. 2
Fig. 2
Ecological model of childhood overweight.
Fig. 3
Fig. 3
Neuroendocrine control of appetite. Solid arrows represent stimulation, and dotted lines represent inhibition. AgRP, agouti-related peptide; CART, cocaine-amphetamine–regulated transcript; CCK, cholecystokinin; CRH, corticotrophin-releasing hormone; MCH, melanocortin hormone; α-MSH, alpha-melanocyte–stimulating hormone; NPY, neuropeptide Y; POMC, pro-opiomelancortin; TRH, thyrotropin-releasing hormone.
See this image and copyright information in PMC

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