Abstract: Environmental factors during early life in development have been shown to influence the susceptibility to develop diseases in later life. In particular, there is a wealth of evidence from both epidemiological and animal studies for greater effect on an offspring′s risk of developing adult chronic diseases （including hypertension, diabetes, coronary
artery disease, obesity, et al） as a result of unbalanced maternal nutrition, ranging from poor to rich environments. These findings indicate new bridges of causality, inferring the possibility of early establishment of persistent metabolic and physiological adjustments that determine morbid outcomes throughout life, grouped as the developmental origins of health and disease（DOHaD）. The mechanisms by which nutritional insults during a period of developmental plasticity
result in adult metabolic phenotype are now beginning to receive considerable scientific interest, in particular the epigenetic and transcriptional regulation of key metabolic genes in response to nutritional stimuli that mediate persistent changes and an adult metabolic phenotype, a continued and greater understanding of these mechanisms will eventually allow specific interventions, with a favorable impact on the global incidence of cardiovascular disease and type 2 diabetes in the future.

Key words: Chronic disease, Pregnancy, Epigenesis, genetic, Embryonic and fetal development, Animal experimentation, Metabolic syndrome