title: Early life programming of obesity.
abstract: As the prevalence of obesity increases across the globe, vast efforts are being directed towards understanding the origins of obesity and mechanisms underlying this rapid increase. It is well known that the current environment of an individual can affect body weight, however, growing evidence suggests that the environment in very early life may be particularly important in determining long term obesity risk. This was prompted by a series of epidemiological studies demonstrating a relationship between suboptimal early growth and later risk of obesity. Evidence from human studies as well as animal models have shown that alterations in nutrition and growth in utero and during early postnatal life can have permanent effects on systems mediating regulation of energy balance. Rapid postnatal growth in particular has been associated with increased risk of developing obesity while slower postnatal growth lowers this risk. Alterations in pathways mediating energy homeostasis have been associated with both patterns of early growth. These include changes in structure and function of neuronal pathways in the brain which lead to deregulation of pathways mediating energy balance. In addition to the alterations at the central level, early nutrition can have detrimental long-lasting effects on peripheral physiological systems, for example the storage of fat and utilization of nutrients that make an individual more prone to development of obesity. The fundamental mechanisms underlying these programmed changes are still to be fully defined, although epigenetic mechanisms may play an important role.
authors.affiliation: University of Cambridge Metabolic Research Laboratories, Cambridge, UK.
authors.forename: Malgorzata S
authors.initials: MS
authors.lastname: Martin-Gronert
authors.forename: Susan E
authors.initials: SE
authors.lastname: Ozanne
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D004195:Disease Models, Animal; D004734:Energy Metabolism; D044127:Epigenesis, Genetic; D006706:Homeostasis; D006801:Humans; D009765:Obesity / Q000453:epidemiology* / Q000503:physiopathology*; D012307:Risk Factors