Endocrine Abstracts

The pituitary lactogenic hormone prolactin (PRL) has well recognized role on metabolism and energy homeostasis, besides the classic physiological actions in lactation and reproduction in humans and rodents. Both persistent hyperprolactinemia (>25 μg/l) and low PRL levels (<7 μg/l) have negative impact on metabolism, indicating the complexity of PRL to the control of metabolism. Although it is known that prolactin may indirectly influence the control of energy homeostasis by causing hypothalamic leptin insensitivity, it has not been reported whether PRL has a direct effect on cellular respiration of hypothalamic neurons, which we hypothesise that may alter the energy sensing mechanism of hypothalamic cells, causing alteration to central control of the metabolism. Preliminary tests of dosage and duration for PRL treatment of immortalised hypothalamic cells mHypoE-37 were performed to establish the optimal protocol to mimic hyperprolactinemia. The chronic treatment for 3 consecutive days with PRL at 300ng/ml and 400ng/ml had robust effects, observed by the increased gene expression of PRLR and STAT5. These chronic treatments decreased the basal respiration of the cells subjected to a Glucose/Pyruvate Oxidation Stress in the Seahorse� apparatus. The oxygen consumption rate (OCR) was maintained lower after a surplus acute injection of PRL. Chronic treatment with PRL has also decreased the ATP production, as observed during the challenge with the ATP synthase inhibitor oligomycin, and the maximal oxygen consumption triggered by FCCP. These preliminary results suggest that PRL may alter the cellular respiration of hypothalamic neurons, although further investigation is required.