“Increased leptin and leptin receptor expression, signal transduction activation and protein synthesis in placenta from pregnant women with gestational diabetes mellitus”

A PÉREZ PÉREZ; F SÁNCHEZ JIMENEZ; J MAYMÓ; Y GAMBINO; JL DUEÑAS; C VARONE; V SÁNCHEZ MARGALET

Geilo

Congreso; International Federation of Placenta Associations (IFPA) Meeting 2011; 2011

International Federation of Placenta Associations (IFPA)

Gestational diabetes is the most frequent pathophysiological process associated with pregnancy, which increases the risk for perinatal morbidity and mortality. These patients have insulin resistance and high plasma levels of insulin and leptin. Placentas from gestational diabetes suffer from structural and functional changes including overgrowth. OBJECTIVES: Since we have recently found that leptin stimulates protein synthesis by activating protein signaling machinery, we aimed to study the expression of leptin and leptin receptor, as well as the leptin receptor activation that may correlate with protein synthesis in placenta from pregnant women with gestational diabetes in comparison with placenta from normal pregnancy. METHODS: We have studied ten placentas from normal pregnancy and ten from patients with gestational diabetes. We measured leptin and leptin receptor expression by quantitative real time-PCR and western blot. We studied leptin receptor signaling by immunoblot using antibodies that recognizes activation of signaling proteins, ie. STAT-3, ERK, PKB, and the activation of different proteins of the initiation stage of translation (S6 Kinase, EIF4EBP1 and EIF4E), and the rate of protein synthesis was assessed by [3H]leucine incorporation experiments. RESULTS: We have found that leptin and leptin receptor are upregulated, and the translation machinery is activated in placentas from gestational diabetes compared with normal pregnancies. Moreover, protein synthesis rate was also found to be increased in placentas from gestational diabetes. CONCLUSION: These results provide new data to understand the molecular mechanisms underlying the increased growth of placenta in gestational diabetes.