Leptin modulates nitric oxide production and lipid metabolism in human placenta
Verónica White A , Elida González A , Evangelina Capobianco A , Carolina Pustovrh A , Nora Martínez A , Romina Higa A , Mario Baier B and Alicia Jawerbaum A CA Laboratory of Reproduction and Metabolism, CEFYBO-CONICET, School of Medicine, University of Buenos Aires, Paraguay 2155 (1121) Buenos Aires, Argentina.
B Obstetrics Department, Carlos G. Durand Hospital, Diaz Velez 5044 (1045) Buenos Aires, Argentina.
C Corresponding author. Email: a.jawerbaum@abaconet.com.ar
Reproduction, Fertility and Development 18(4) 425-432 https://doi.org/10.1071/RD05105
Submitted: 15 September 2005 Accepted: 1 January 2006 Published: 22 March 2006
Abstract
Leptin has significant effects on appetite, energy expenditure, lipid mobilisation and reproduction. During pregnancy, leptin is produced in the placenta, a tissue in which leptin receptors are highly expressed, suggesting autocrine/paracrine functions for 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 levels of triglycerides (P < 0.01) and cholesterol (P < 0.001) in term human placenta. The effect of leptin on lipid mass seems to be independent of the modulation of de novo lipid synthesis because leptin did not modify the incorporation of 14C-acetate into any of the lipids evaluated. We investigated the effects of leptin on placental lipid catabolism and found that in both term human placental explants and primary cultures of trophoblastic cells, leptin increased glycerol release, an index of the hydrolysis of esterified lipids, in a dose-dependent manner. In conclusion, we have shown that leptin affects NO production and lipid catabolism in human placenta, providing supportive evidence for a role of leptin in placental functions that would determine the transfer of nutrients to the developing fetus.
Acknowledgments
The authors thank Dr Fernando Larrea, Lorenza Díaz and Alina Oknianska for advice on the trophoblast culture and lipid catabolism evaluation techniques. The authors also thank María Ester Castro for her helpful technical assistance. This work was supported by grants from Agencia de Promoción Científica y Tecnológica de Argentina (PICT 05 10652; to EG and AJ), from Consejo Nacional de Investigaciones Científicas y Técnicas (PIP 5397/05; to AJ) and from PLACIRH (PLC-269/2001; to VW).
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