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      Acute stress inhibits food intake and alters ghrelin signaling in the brain of tilapia (Oreochromis mossambicus).

      Domestic Animal Endocrinology
      Animals, Brain, metabolism, Corticotropin-Releasing Hormone, biosynthesis, genetics, Eating, physiology, Female, Ghrelin, blood, Male, Neuropeptide Y, RNA, Messenger, chemistry, Random Allocation, Receptors, Ghrelin, Reverse Transcriptase Polymerase Chain Reaction, veterinary, Signal Transduction, Stress, Physiological, Tilapia

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          Abstract

          This study investigated the effect of an acute stress on food intake and on the expression of neuropeptide Y (NPY), corticotropin-releasing hormone (CRH), and ghrelin and its receptors, growth hormone secretagogue receptors (GHSRs) in the tilapia (Oreochromis mossambicus). Food intake was significantly (P < 0.01) reduced in fish after a 30-min crowding and handling stress. In a second group of animals exposed to the same 30-min stressor, tissue samples were collected immediately after the stressor to determine changes in the neuroendocrine regulators of food intake. Although CRH and NPY are considered the major mediators of appetite during stress, both mRNA levels were unaltered in the telencephalon/pre-optic area and in the hypothalamic/optic tectum. Interestingly, there was an elevation in the ghrelin transcript (P < 0.05) in the telencephalon/pre-optic area and elevation of its functional receptor (GHSR1a-LR) (P < 0.001) in the hypothalamic/optic tectum. Elevation of GHSR-LR heteronuclear RNA (P < 0.01) in the telencephalon/pre-optic area and suppression in the hypothalamic/optic tectum (P < 0.001) suggest rapid control of the ghrelin regulatory system in response to acute stress. These results suggest that ghrelin signaling is altered during acute stress. It is not clear if these changes result in altered feeding behavior because no changes in CRH or NPY mRNA expression were observed or if ghrelin is playing a role in regulating overall metabolic changes after acute stress. Copyright © 2013 Elsevier Inc. All rights reserved.

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