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. Gestational diabetes mellitus 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.
GESTATIONAL DIABETES MELLITUS INTERFERESWITH THE BIOLOGICAL CHARACTERISTICS OFWHARTON'S JELLY MESENCHYMAL STEM CELLS.
LANUTI, PAOLA;PIERDOMENICO, Laura;LACHMANN, Raskit;VITACOLONNA, Ester;MARCHISIO, Marco;MISCIA, Sebastiano
2011-01-01
Abstract
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. Gestational diabetes mellitus 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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
