Resumo

FAINGOLD, MC. Epigenetic Factors in Pregnant Women with Diabetes. Rev. argent. endocrinol. metab. [online]. 2014, vol.51, n.3, pp.151-159. ISSN 1851-3034.

It is now accepted that offspring exposed to maternal undernutrition, obesity, or gestational diabetes mellitus (GDM) have an increased risk for chronic diseases later in life, supporting the theory of the early origin of chronic diseases. The main adverse outcome on progenies from pregnancy complicated with maternal diabetes appears to be macrosomia, and it is well known that intrauterine exposure to hyperglycemia usually increases the risk and misprograms the offspring to develop diabetes and/or obesity at adulthood. This “fetal programming”, due to intrauterine diabetic milieu, is called “metabolic memory”. Furthermore, there is evidence that maternal obesity may also increase the risk of obesity and diabetes in the offspring. However, offspring born to women with GDM possibly exhibit a greater development of macrosomia than that born to obese women. Obesity and GDM have independent and additive effects. However, the molecular mechanisms through which the offspring exposure to an altered in utero environment translates into the development of chronic metabolic diseases are not yet well understood. Recent reports suggest that epigenetic modifications are a potential mechanism for fetal metabolic misprogramming. This review provides an overview of the relationship between the exposure to an altered intrauterine environment and fetal metabolic misprogramming with special emphasis on gestational diabetes mellitus and epigenetic variations, and on how these early epigenetically-related changes program the offspring predisposition for the development of obesity and type 2 diabetes mellitus later in life. Rev Argent Endocrinol Metab 51:151-159, 2014 No financial conflicts of interest exist.

Palavras-chave : Gestational diabetes; Epigenetics; Programming; Intrauterine enviroment; Offspring.

        · resumo em Espanhol     · texto em Espanhol     · Espanhol ( pdf )