Leptin modulates nitric oxide production and lipid metabolism in human placenta.

WHITE, VERÓNICA; ELIDA TERESA GONZALEZ; CAPOBIANCO, EVANGELINA; PUSTOVRH, CAROLINA; NORA MARTÍNEZ; HIGA, R.; BAIER, M.; JAWERBAUM, ALICIA

REPRODUCTION FERTILITY AND DEVELOPMENT

Commonwealth Scientific And Industrial Research Organization (Csiro)

Año: 2006 vol. 18 p. 425 - 432

1031-3613

Leptin has significant effects on appetite, energy expenditure, lipid mobilization and reproduction. During pregnancy, leptin is produced in the placenta, a tissue where leptin receptors are highly expressed, suggesting autocrine/paracrine functions of this hormone. In the present study, a putative role of leptin as a regulator of nitric oxide (NO) production and lipid metabolism was evaluated in term human placenta. We demonstrated that leptin enhanced NO production in human placental explants (p<0.01). Although leptin did not modify the placental levels of cholesteryl esters and phospholipids, leptin decreased triglycerides (p<0.01) and cholesterol levels (p<0.001) in term human placenta. As leptin did not modify incorporation of 14C-acetate to any of the lipids evaluated, leptin effects on lipid mass seems to be independent of the modulation of the de novo lipid synthesis. We tested leptin effects on placental lipid catabolism and found that both in term human placental explants and in primary cultures of trophoblastic cells leptin increases glycerol release, an index of hydrolysis of esterified lipids, in a dose-dependent manner. In conclusion, we demonstrated leptin effects on NO production and lipid catabolism in human placenta, providing supportive evidence of a role of leptin in placental functions that condition the transfer of nutrients to the developing fetus.