Early life programming of obesity and metabolic disease.
It is becoming increasingly apparent that conditions experienced in early life play an important role in the long-term health of individuals. Alterations in development due to impaired, excessive or imbalanced growth, both in utero and during critical periods of relative plasticity beyond birth, can lead to the permanent programming of physiological systems. The regulation of energy balance is one area that is receiving particular attention, as rates of obesity and associated metabolic and cardiovascular disease continue to rise. Over recent decades, much progress has been made toward understanding the way in which metabolic tissues and physiological systems develop, and the impact of early life events and nutrition on these processes. It is apparent within human populations that some individuals are better able to maintain an appropriate body weight in the face of an obesogenic environment. Animal models have been widely used for the investigation of differential susceptibility to diet-induced obesity (DIO) and impaired energy balance regulation, and are shedding light on key pathways that may be involved. Alterations in pathways mediating energy homeostasis, outlined below, are likely candidates for programming effects following disturbed growth in early life.
D000273:Adipose Tissue / Q000254:growth & development / Q000502:physiology; D000818:Animals; D004032:Diet; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000502:physiology; D005260:Female; D005938:Glucocorticoids / Q000502:physiology; D006128:Growth / Q000502:physiology; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D020738:Leptin / Q000502:physiology; D008659:Metabolic Diseases / Q000503:physiopathology*; D009765:Obesity / Q000503:physiopathology*; D044343:Overnutrition / Q000503:physiopathology; D010641:Phenotype; D011247:Pregnancy
D005938:Glucocorticoids; D020738:Leptin