Type 2 diabetes mellitus (T2DM) is a multifactorial disease, and its aetiology involves a complex interplay between genetic,\r\nepigenetic, and environmental factors. In recent years, evidences from both human and animal experiments have correlated\r\nearly life factors with programming diabetes risk in adult life. Fetal and neonatal period is crucial for organ development. Many\r\nmaternal factors during pregnancy may increase the risk of diabetes of offsprings in later life, which include malnutrition, healthy\r\n(hyperglycemia and obesity), behavior (smoking, drinking, and junk food diet), hormone administration, and even stress. In\r\nneonates, catch-up growth, lactation, glucocorticoids administration, and stress have all been found to increase the risk of insulin\r\nresistance or T2DM.Unfavorable environments (socioeconomic situation and famine) or obesity also has long-termnegative effects\r\non children by causing increased susceptibility to T2DMin adults.We also address the potential mechanisms thatmay underlie the\r\ndevelopmental programming of T2DM. Therefore, it might be possible to prevent or delay the risk for T2DM by improving preand/\r\nor postnatal factors.
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