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      The Changes They are A-Timed: Metabolism, Endogenous Clocks, and the Timing of Puberty

      review-article
      1 , 1
      Frontiers in Endocrinology
      Frontiers Research Foundation
      obesity, kisspeptin, circadian, puberty, GnRH

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          Abstract

          Childhood obesity has increased dramatically over the last several decades, particularly in industrialized countries, often accompanied by acceleration of pubertal progression and associated reproductive abnormalities (Biro et al., 2006; Rosenfield et al., 2009). The timing of pubertal initiation and progression in mammals is likely influenced by nutritional and metabolic state, leading to the hypothesis that deviations from normal metabolic rate, such as those seen in obesity, may contribute to observed alterations in the rate of pubertal progression. While several recent reviews have addressed the effects of metabolic disorders on reproductive function in general, this review will explore previous and current models of pubertal timing, outlining a potential role of endogenous timing mechanisms such as cellular circadian clocks in the initiation of puberty, and how these clocks might be altered by metabolic factors. Additionally, we will examine recently elucidated neuroendocrine regulators of pubertal progression such as kisspeptin, explore models detailing how the mammalian reproductive axis is silenced during the juvenile period and reactivated at appropriate developmental times, and emphasize how metabolic dysfunction such as childhood obesity may alter timing cues that advance or delay pubertal progression, resulting in diminished reproductive capacity.

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          Most cited references211

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          Positional cloning of the mouse obese gene and its human homologue.

          The mechanisms that balance food intake and energy expenditure determine who will be obese and who will be lean. One of the molecules that regulates energy balance in the mouse is the obese (ob) gene. Mutation of ob results in profound obesity and type II diabetes as part of a syndrome that resembles morbid obesity in humans. The ob gene product may function as part of a signalling pathway from adipose tissue that acts to regulate the size of the body fat depot.
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            Identification and expression cloning of a leptin receptor, OB-R.

            The ob gene product, leptin, is an important circulating signal for the regulation of body weight. To identify high affinity leptin-binding sites, we generated a series of leptin-alkaline phosphatase (AP) fusion proteins as well as [125I]leptin. After a binding survey of cell lines and tissues, we identified leptin-binding sites in the mouse choroid plexus. A cDNA expression library was prepared from mouse choroid plexus and screened with a leptin-AP fusion protein to identify a leptin receptor (OB-R). OB-R is a single membrane-spanning receptor most related to the gp130 signal-transducing component of the IL-6 receptor, the G-CSF receptor, and the LIF receptor. OB-R mRNA is expressed not only in choroid plexus, but also in several other tissues, including hypothalamus. Genetic mapping of the gene encoding OB-R shows that it is within the 5.1 cM interval of mouse chromosome 4 that contains the db locus.
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              Molecular components of the mammalian circadian clock.

              Circadian rhythms are approximately 24-h oscillations in behavior and physiology, which are internally generated and function to anticipate the environmental changes associated with the solar day. A conserved transcriptional-translational autoregulatory loop generates molecular oscillations of 'clock genes' at the cellular level. In mammals, the circadian system is organized in a hierarchical manner, in which a master pacemaker in the suprachiasmatic nucleus (SCN) regulates downstream oscillators in peripheral tissues. Recent findings have revealed that the clock is cell-autonomous and self-sustained not only in a central pacemaker, the SCN, but also in peripheral tissues and in dissociated cultured cells. It is becoming evident that specific contribution of each clock component and interactions among the components vary in a tissue-specific manner. Here, we review the general mechanisms of the circadian clockwork, describe recent findings that elucidate tissue-specific expression patterns of the clock genes and address the importance of circadian regulation in peripheral tissues for an organism's overall well-being.
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                Author and article information

                Journal
                Front Endocrinol (Lausanne)
                Front Endocrinol (Lausanne)
                Front. Endocrin.
                Frontiers in Endocrinology
                Frontiers Research Foundation
                1664-2392
                28 March 2012
                2012
                : 3
                : 45
                Affiliations
                [1] 1simpleDepartment of Biomedical Sciences, College of Veterinary Medicine, Oregon State University Corvallis, OR, USA
                Author notes

                Edited by: Carol F. Elias, University of Texas Southwestern Medical Center, USA

                Reviewed by: Lance Kriegsfeld, University of California, USA; Gloria E. Hoffman, Morgan State University, USA

                *Correspondence: Patrick E. Chappell, Department of Biomedical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis, OR 97331, USA. e-mail: patrick.chappell@ 123456oregonstate.edu

                Present address: Kristen P. Tolson, Department of Reproductive Medicine, University of California San Diego, La Jolla, CA 92093, USA.

                This article was submitted to Frontiers in Systems and Translational Endocrinology, a specialty of Frontiers in Endocrinology.

                Article
                10.3389/fendo.2012.00045
                3355854
                22645521
                002deeb3-1044-4350-85d0-f45439922212
                Copyright © 2012 Tolson and Chappell.

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.

                History
                : 07 September 2011
                : 08 March 2012
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 248, Pages: 17, Words: 19087
                Categories
                Endocrinology
                Review Article

                Endocrinology & Diabetes
                obesity,circadian,puberty,kisspeptin,gnrh
                Endocrinology & Diabetes
                obesity, circadian, puberty, kisspeptin, gnrh

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