摘要
The concept “fetal programming” shows who still in the intrauterine life, can interfere in factors related to the genesis and development of diseases in childhood, adolescence and adult life. The literature shows that children born to mothers with gestational diabetes mellitus (GDM) are at increased risk for the development of obesity in adulthood, it becomes fundamental to study more about the subject. Obesity is a disease of multifactorial etiology, resulting from complex interactions between genetic and environmental factors. However, the marked increase in its incidence, precocity and severity are not yet fully understood. Several findings suggest that stressor stimuli (e.g. diabetes, nutritional changes) during intrauterine development may promote epigenetic changes, as well as affect mitochondrial metabolism, which may modulate fetal development and predispose to the late development of diseases. Despite the considerable amount of evidence accumulated about intrauterine programming for diseases of adult life, the determinant mechanisms of such programming are not yet clear.
The concept “fetal programming” shows who still in the intrauterine life, can interfere in factors related to the genesis and development of diseases in childhood, adolescence and adult life. The literature shows that children born to mothers with gestational diabetes mellitus (GDM) are at increased risk for the development of obesity in adulthood, it becomes fundamental to study more about the subject. Obesity is a disease of multifactorial etiology, resulting from complex interactions between genetic and environmental factors. However, the marked increase in its incidence, precocity and severity are not yet fully understood. Several findings suggest that stressor stimuli (e.g. diabetes, nutritional changes) during intrauterine development may promote epigenetic changes, as well as affect mitochondrial metabolism, which may modulate fetal development and predispose to the late development of diseases. Despite the considerable amount of evidence accumulated about intrauterine programming for diseases of adult life, the determinant mechanisms of such programming are not yet clear.
