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      Endocrine Regulation of Compensatory Growth in Fish

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          Abstract

          Compensatory growth (CG) is a period of accelerated growth that occurs following the alleviation of growth-stunting conditions during which an organism can make up for lost growth opportunity and potentially catch up in size with non-stunted cohorts. Fish show a particularly robust capacity for the response and have been the focus of numerous studies that demonstrate their ability to compensate for periods of fasting once food is made available again. CG is characterized by an elevated growth rate resulting from enhanced feed intake, mitogen production, and feed conversion efficiency. Because little is known about the underlying mechanisms that drive the response, this review describes the sequential endocrine adaptations that lead to CG; namely during the precedent catabolic phase (fasting) that taps endogenous energy reserves, and the following hyperanabolic phase (refeeding) when accelerated growth occurs. In order to elicit a CG response, endogenous energy reserves must first be moderately depleted, which alters endocrine profiles that enhance appetite and growth potential. During this catabolic phase, elevated ghrelin and growth hormone (GH) production increase appetite and protein-sparing lipolysis, while insulin-like growth factors (IGFs) are suppressed, primarily due to hepatic GH resistance. During refeeding, temporal hyperphagia provides an influx of energy and metabolic substrates that are then allocated to somatic growth by resumed IGF signaling. Under the right conditions, refeeding results in hyperanabolism and a steepened growth trajectory relative to constantly fed controls. The response wanes as energy reserves are re-accumulated and homeostasis is restored. We ascribe possible roles for select appetite and growth-regulatory hormones in the context of the prerequisite of these catabolic and hyperanabolic phases of the CG response in teleosts, with emphasis on GH, IGFs, cortisol, somatostatin, neuropeptide Y, ghrelin, and leptin.

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          Leptin.

          The discovery of the adipose-derived hormone leptin has generated enormous interest in the interaction between peripheral signals and brain targets involved in the regulation of feeding and energy balance. Plasma leptin levels correlate with fat stores and respond to changes in energy balance. It was initially proposed that leptin serves a primary role as an anti-obesity hormone, but this role is commonly thwarted by leptin resistance. Leptin also serves as a mediator of the adaptation to fasting, and this role may be the primary function for which the molecule evolved. There is increasing evidence that leptin has systemic effects apart from those related to energy homeostasis, including regulation of neuroendocrine and immune function and a role in development.
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            Compensatory growth in fishes: a response to growth depression

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              The role of neuropeptide Y in the antiobesity action of the obese gene product.

              Recently Zhang et al. cloned a gene that is expressed only in adipose tissue of the mouse. The obese phenotype of the ob/ob mouse is linked to a mutation in the obese gene that results in expression of a truncated inactive protein. Human and rat homologues for this gene are known. Previous experiments predict such a hormone to have a hypothalamic target. Hypothalamic neuropeptide Y stimulates food intake, decreases thermogenesis, and increases plasma insulin and corticosterone levels making it a potential target. Here we express the obese protein in Escherichia coli and find that it suppresses food intake and decreases body weight dramatically when administered to normal and ob/ob mice but not db/db (diabetic) mice, which are thought to lack the appropriate receptor. High-affinity binding was detected in the rat hypothalamus. One mechanism by which this protein regulated food intake and metabolism was inhibition of neuropeptide-Y synthesis and release.
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                Author and article information

                Journal
                Front Endocrinol (Lausanne)
                Front Endocrinol (Lausanne)
                Front. Endocrinol.
                Frontiers in Endocrinology
                Frontiers Media S.A.
                1664-2392
                01 July 2013
                2013
                : 4
                : 74
                Affiliations
                [1] 1Department of Biology, North Carolina State University , Raleigh, NC, USA
                Author notes

                Edited by: Yong Zhu, East Carolina University, USA

                Reviewed by: Weimin Zhang, Sun Yat-sen University, China; Wanshu Hong, Xiamen University, China; Takeshi Miura, South Ehime Fisheries Research Center, Japan

                *Correspondence: Russell J. Borski, Department of Biology, North Carolina State University, Box 7617, Raleigh, NC 27695, USA e-mail: russell˙borski@ 123456ncsu.edu

                This article was submitted to Frontiers in Experimental Endocrinology, a specialty of Frontiers in Endocrinology.

                Article
                10.3389/fendo.2013.00074
                3696842
                23847591
                c7ad6add-553d-4e24-8028-0c39455cf339
                Copyright © 2013 Won and Borski.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.

                History
                : 08 February 2013
                : 06 June 2013
                Page count
                Figures: 2, Tables: 1, Equations: 0, References: 181, Pages: 13, Words: 12829
                Categories
                Endocrinology
                Review Article

                Endocrinology & Diabetes
                compensatory growth,fish,aquaculture,growth hormone,ghrelin,npy,leptin,insulin-like growth factor

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