Recent research indicates that the origin of obesity and related metabolic disorders is not only caused by
genetic and risk factors in adult life (unbalanced diet, insufficient physical activity) but also may be influenced by the
perinatal environment. In addition, studies in animal models suggest that the mesenchymal stem cell commitment into
pre-adipocytes can already occur during fetal development and perinatal life. Since the number of pre-adipocytes and
mature adipocytes is lower in normal subjects than in obese subjects, changes in the prenatal maturational process may
play a role in the pathogenesis of obesity and metabolic-associated diseases. Hyperglycemia during pregnancy is related to
an increased risk of obesity, early onset of metabolic syndrome and type 2 diabetes in the offspring. For this reason it
would be useful to investigate how the perinatal environment may affect fetal mesenchymal stem cells, especially in
deregulated gestational diabetes, where the fetal environment is modified in terms of hormone levels and nutrition.
Therefore, we have compared Wharton's jelly mesenchymal stem cells (WJ-MSC) obtained from umbilical cord of both
healthy and diabetic mothers, in order to better understand the mechanisms involved in metabolic diseases in offspring of
diabetic mothers. Results indicate that WJ-MSC from diabetic mothers display, in contrast to cells from healthy mothers,
a higher ability to differentiate towards the adipogenic lineage. This suggests that the diabetic uterine environment may be
responsible for a “pre-commitment” that could give rise in the post natal life to an alteration of adipocyte production upon
an incorrect diet style, which in turn would produce obesity.