[Programming nutritional and metabolic disorders: the diabetic environment during gestation].
During the last years, obesity and subsequent metabolic disorders and cardiovascular diseases have tremendously increased. Recent studies have shown that risk factors of cardiovascular diseases appear as soon as in infancy. In many situations, these disorders are programmed in early life during fetal development. These observations have lead to the concept of programming. The first studies on this subject underlined the link between poor fetal growth and the risk of nutritional and metabolic disorders during adulthood. But, it is now evident that excess of fetal growth as it is observed during pregnancy with maternal diabetes leads to the same consequences. The metabolic syndrome or syndrome X is the name for a clustering of risk factors for cardiovascular diseases and type II diabetes that are of metabolic origin. This syndrome, first described in the adults, is more and more studied during childhood and adolescence. Metabolic syndrome is now described in youth, particularly in subjects with risk factors as obesity. Alterations of intra-uterine environment lead to modified early development and represent short-term adaptations transmitted from one generation to another. This intergeneration effect contributes to the burden of adult metabolic disorders and cardiovascular diseases, as seen in the last decades. There is considerable evidence for the contribution of epigenetic mechanisms for the lifelong and the intergenerational alteration of gene transcription by variation in the early life environment. One of the major challenges in the following years is to promote public health programs which are aimed at prevention of long-term consequences of fetal programming.
Motte
E
E
Service d'endocrinologie et de diabétologie, hôpital Saint-Vincent-de-Paul, AP-HP, Paris, France.
Beauval
B
B
Laurent
M
M
Melki
I
I
Schmit
A
A
Vottier
G
G
Mitanchez
D
D
D000293:Adolescent; D000328:Adult; D002318:Cardiovascular Diseases / Q000175:diagnosis* / Q000235:genetics; D002648:Child; D015362:Child Nutrition Disorders / Q000175:diagnosis* / Q000235:genetics; D002675:Child, Preschool; D003924:Diabetes Mellitus, Type 2 / Q000175:diagnosis* / Q000235:genetics; D016640:Diabetes, Gestational / Q000175:diagnosis* / Q000235:genetics; D044127:Epigenesis, Genetic / Q000235:genetics; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005838:Genotype; D006801:Humans; D007223:Infant; D007333:Insulin Resistance; D008297:Male; D024821:Metabolic Syndrome / Q000175:diagnosis* / Q000235:genetics; D009765:Obesity / Q000175:diagnosis* / Q000235:genetics; D010641:Phenotype; D011247:Pregnancy; D012307:Risk Factors