Summary
Pregnancy is a hypermetabolic state in which a great increase in maternal body fat and weight occurs, mostly in the final trimester of gestation, and it is associated with relevant neuroendocrine changes as adaptations to the new hormonal status. Data gleaned over the last few years have allowed the characterization of different central and peripheral signals involved in the regulation of body weight homeostasis.
Serum leptin levels were significantly increased during rat gestation. Leptin mRNA levels in both the adipose tissue and placenta were higher as pregnancy progressed, suggesting a role for both tissues in the hyperproduction of leptin. This paradoxical increase in leptin concentration during gestation suggests that a physiological state of leptin resistance may exist at the hypothalamic level that may explain the hyperphagia observed in pregnant rats. A specific reduction of the mRNA levels encoding the leptin receptor isoform Ob-Rb in the hypothalamus of pregnant rats in comparison to non-pregnant animals suggests that, during pregnancy, the hypothalamus shows a physiological resistance to the high levels of leptin due, at least in part, to a decrease in the expression of the long, biologically active form of the leptin receptor (Ob-Rb). During lactation an increased expression of some of the short forms of the leptin receptor (Ob-Re and Ob-Rf) was found. This increase could contribute to the hyperphagia present during lactation. Finally, Neuropeptide (NPY)mRNA levels in the arcuate nucleus were increased during pregnancy and lactation whereas melanin-concentrating hormone (MCH) and preprorexin levels were decreased. Therefore, it is possible that NPY could also be one of the adaptive mechanisms that take place during pregnancy and lactation in order to meet increased metabolic requirements.
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García, M.C. et al. (2002). Regulation of Body Weight Homeostasis During Pregnancy and Lactation. In: Kordon, C., Robinson, I., Hanoune, J., Dantzer, R., Christen, Y. (eds) Brain Somatic Cross-Talk and the Central Control of Metabolism. Research and Perspectives in Endocrine Interactions. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-18999-9_7
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DOI: https://doi.org/10.1007/978-3-642-18999-9_7
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