Circulating but not CSF, ghrelin is involved in food intake in sheep

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Cold-induced glutamate release in vivo from the magnocellular region of the paraventricular nucleus is involved in ovarian sympathetic activation

We previously reported that centrally-induced sympathetic activation in response to cold stress is associated with a polycystic ovarian condition in rats, and thyrotrophin-releasing hormone (TRH) released locally from the magnocellular region of the paraventricular nucleus (PVN) appears to be involved in this activation. Because TRH neurones express NMDA glutamate receptors, in the present study, we investigated the role of glutamate in the increased release of TRH from magnocellular neurones induced by cold stress and its relationship to ovarian neurotransmission. Animals with a push-pull cannula stereotaxically implanted into the magnocellular portion of the PVN were exposed to cold stress (4 degrees C for 64 h) and subjected to intracerebral perfusion. Perfusate fractions were obtained and analysed by high-performance liquid chromatography to measure glutamate and GABA levels. Glutamate, but not GABA, release increased significantly in animals perfused under cold exposure. In vivo administration of glutamate to the PVN increased TRH release. Injection of MK-801 into the magnocellular portion of the PVN reduced ovarian noradrenaline turnover and led to an increase in catecholamine concentration from the adrenal glands and celiac ganglia. Taken together, the results obtained in the present study strongly suggest that glutamate release from the magnocellular PVN is sensitive to cold stress and that glutamate acts through the NMDA receptor to mediate cold-induced TRH release. This in turn triggers hypothalamic-ovarian pathway activation, which might be responsible for the polycystic condition induced by cold stress and other ovarian pathologies characterised by increased sympathetic discharge

Ghrelin acylation by ghrelin-O-acyltransferase can occur in healthy part of oncologic liver in humans

INTRODUCTION: Activation of ghrelin is controlled by the enzyme Ghrelin-O-Acyl Transferase (GOAT). In humans, localization of this acylation is poorly understood. The aim of that study was to explore GOAT localization and activation in human Liver by evaluating both bioactive and non-bioactive ghrelin in the blood stream entering and leaving liver and to simultaneously evaluate GOAT mRNA expression in Liver. METHODS: Healthy part of oncologic hepatic tissue collected from nine patients undergoing hepatectomy was used to evaluate GOAT mRNA expression by quantitative real time polymerase chain reaction (RTqPCR). Simultaneously blood from portal vein, supra hepatic vein, sub clavicular vein and radial artery was also sampled to assay total and acylated ghrelin. RESULTS: Acylated ghrelin level was significantly increased in supra hepatic vein compared to portal vein level (385±42 ng/ml vs. 268±24 ng/ml, p=0.04). Supra hepatic vein to portal vein ratio for acylated ghrelin (acylation ratio) is at 1.4±0.1. Mean expression of GOAT mRNA in liver, expressed as 2-∆Ct/µg total RNA/1µl of liver tissue was at 0.042±0.021 arbitrary units. GOAT mRNA expression in liver was correlated with acylated to total ghrelin ratio in supra hepatic vein (p=0.016, R=0.75) and with acylation liver ratio (p=0.05, R=0.61). CONCLUSIONS: Blood concentration of acylated ghrelin was found significantly increased after its passage through liver suggesting acylation can occur in the liver. RTqPCR data confirmed the presence of GOAT in liver, with positive correlation between GOAT expression and acylated ghrelin liver ratio. This study strongly suggests that liver is a site of ghrelin acylation in human

Effect of 17 p estradiol on prolactin secretion and thyroliberin responsiveness in two rat prolactin continuous cell lines. Definition of an experimental model

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