The changes they are a-timed: metabolism, endogenous clocks, and the timing of puberty
- Department of Biomedical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis, OR, USA
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.
Keywords: obesity, kisspeptin, circadian, puberty, GnRH
Citation: Tolson KP and Chappell PE (2012) The changes they are a-timed: metabolism, endogenous clocks, and the timing of puberty. Front. Endocrin. 3:45. doi: 10.3389/fendo.2012.00045
Received: 07 September 2011; Accepted: 08 March 2012;
Published online: 28 March 2012.
Carol F. Elias
, University of Texas Southwestern Medical Center, USA
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.
*Correspondence: Patrick E. Chappell, Department of Biomedical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis, OR 97331, USA. e-mail: firstname.lastname@example.org
†Present address: Kristen P. Tolson, Department of Reproductive Medicine, University of California San Diego, La Jolla, CA 92093, USA.