During pregnancy, rodents and humans show increased food intake and adiposity. Nevertheless, circulating leptin concentration is increased in this situation as well as the hypothalamic expression of the suppressor of cytokine signaling 3 (SOCS3). Thus, pregnancy is an interesting model of leptin resistance because its transitory nature. However, the molecular mechanisms which are responsible for leptin resistance during pregnancy are unknown. A hyper-activation of the prolactin receptor (PrlR) is a potential factor which may be associated with leptin resistance observed in pregnancy. PrlR can be activated by placental lactogens as well. This receptor, just like the leptin receptor (LepR), can induce the phosphorylation of the signal transducer and activators of transcription (STATs) increasing the expression of SOCS3, which in turn can inhibit signaling of LepR. This hypothesis is plausible only if LepR and PrlR are expressed in the same neuronal population. This research aims to identify the brain areas which have cells that co-express prolactin and leptin receptors.
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