Maternal Diabetes in Pregnancy: Early and Long-Term Outcomes on the Offspring and the Concept of “Metabolic Memory”

Figure 1

In GDM, adipose tissue secretes low adiponectin (anti-inflammatory and positive stimulator of insulin sensitizing) and high TNF-α and IL-6 which contribute to inflammatory state and insulin resistance in diabetic pregnancy as well as in macrosomia. Leptin, being pro-inflammatory, is highly produced by adipose tissue during diabetic pregnancy and insulin resistance (experimental study [75]) and implicated in the pathogenesis of weight gain in macrosomic babies. Leptin may exert its effects by interacting with neuropeptide-Y in the hypothalamus. The intrauterine hyperglycemia may act on the fetal hypothalamus and create a kind of “metabolic memory” which programs obesity and metabolic syndrome in the offspring during adulthood. (+) positive regulation (−) negative regulation. NPY, neuropeptide-Y.