Pubertal Onset in Girls is Strongly Influenced by Genetic Variation Affecting FSH Action

Hagen, Casper P; Sørensen, Kaspar; Aksglæde, Lise; Mouritsen, Annette; Mieritz, Mikkel G; Tinggaard, Jeanette; Wohlfart-Veje, Christine; Petersen, Jørgen Holm; Main, Katharina M.; Meyts, Ewa Rajpert‐De; Almstrup, Kristian; Juul, Anders

doi:10.1038/srep06412

Cited by 30 publications

(27 citation statements)

References 48 publications

(65 reference statements)

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“…Furthermore, there is growing evidence that sexual maturation is occurring progressively earlier in the US and some European countries (Euling et al 2008;Aksglaede et al 2009;Biro et al 2013;Cabrera et al 2014). The underlying causes remain unclear although some suggest higher rates of obesity (Biro et al 2013) while others suggest epigenetic and environmental influences (Aksglaede et al 2009;Meeker, 2012;Hagen et al 2014) as the main contributing factors. These variations in pubertal timing further complicate the validity of equating adolescence to puberty.…”

Section: What Is Adolescence?mentioning

confidence: 99%

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Nicotine and the adolescent brain

Yuan¹,

Cross

Loughlin³

et al. 2015

The Journal of Physiology

402

294

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Adolescence encompasses a sensitive developmental period of enhanced clinical vulnerability to nicotine, tobacco, and e-cigarettes. While there are sociocultural influences, data at preclinical and clinical levels indicate that this adolescent sensitivity has strong neurobiological underpinnings. Although definitions of adolescence vary, the hallmark of this period is a profound reorganization of brain regions necessary for mature cognitive and executive function, working memory, reward processing, emotional regulation, and motivated behavior. Regulating critical facets of brain maturation are nicotinic acetylcholine receptors (nAChRs). However, perturbations of cholinergic systems during this time with nicotine, via tobacco or e-cigarettes, have unique consequences on adolescent development. In this review, we highlight recent clinical and preclinical data examining the adolescent brain's distinct neurobiology and unique sensitivity to nicotine. First, we discuss what defines adolescence before reviewing normative structural and neurochemical alterations that persist until early adulthood, with an emphasis on dopaminergic systems. We review how acute exposure to nicotine impacts brain development and how drug responses differ from those seen in adults. Finally, we discuss the persistent alterations in neuronal signaling and cognitive function that result from chronic nicotine exposure, while highlighting a low dose, semi-chronic exposure paradigm that may better model adolescent tobacco use. We argue that nicotine exposure, increasingly occurring as a result of e-cigarette use, may induce epigenetic changes that sensitize the brain to other drugs and prime it for future substance abuse.

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Section: What Is Adolescence?mentioning

confidence: 99%

“…; Meeker, ; Hagen et al . ) as the main contributing factors. These variations in pubertal timing further complicate the validity of equating adolescence to puberty.…”

Section: Introductionmentioning

confidence: 99%

Nicotine and the adolescent brain

Yuan¹,

Cross

Loughlin³

et al. 2015

The Journal of Physiology

402

294

View full text Add to dashboard Cite

show abstract

“…In humans, genes have been identified in which variants influence the age of onset of puberty. These include the follicle-stimulating hormone (FSH) receptor [87] and vestigial-like family member 3 (vgll3) [88] that also affects timing of puberty in Atlantic salmon ( Salmo salar ) [88]. There is some evidence that fish at contaminated sites have altered life cycles.…”

Section: Physiological Mechanisms For Adaptations and Their Potentialmentioning

confidence: 99%

Adaptive capabilities and fitness consequences associated with pollution exposure in fish

Hamilton

Rolshausen

Webster

et al. 2017

Phil. Trans. R. Soc. B

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Many fish populations are exposed to harmful levels of chemical pollution and selection pressures associated with these exposures have led to the evolution of tolerance. Our understanding of the physiological basis for these adaptations is limited, but they are likely to include processes involved with the absorption, distribution, metabolism and/or excretion of the target chemical. Other potential adaptive mechanisms include enhancements in antioxidant responses, an increased capacity for DNA and/or tissue repair and alterations to the life cycle of fish that enable earlier reproduction. Analysis of single-nucleotide polymorphism frequencies has shown that tolerance to hydrocarbon pollutants in both marine and estuarine fish species involves alteration in the expression of the xenobiotic metabolism enzyme CYP1A. In this review, we present novel data showing also that variants of the CYP1A gene have been under selection in guppies living in Trinidadian rivers heavily polluted with crude oil. Potential costs associated with these adaptations could reduce fitness in unpolluted water conditions. Integrating knowledge of local adaptation to pollution is an important future consideration in conservation practices such as for successful restocking, and improving connectivity within river systems.This article is part of the themed issue ‘Human influences on evolution, and the ecological and societal consequences’.

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“…To analyze the age at VO, a Cox regression model was applied. This model is an adaptation of probit analyses commonly used to study pubertal onset in humans (33). Probit analysis is a type of regression used with binomial response variable (in this study: VO, yes/no).…”

Section: Statisticsmentioning

confidence: 99%

Delayed Neuroendocrine Sexual Maturation in Female Rats After a Very Low Dose of Bisphenol A Through Altered GABAergic Neurotransmission and Opposing Effects of a High Dose

et al. 2016

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Rat sexual maturation is preceded by a reduction of the interpulse interval (IPI) of GnRH neurosecretion. This work aims at studying disruption of that neuroendocrine event in females after early exposure to a very low dose of bisphenol A (BPA), a ubiquitous endocrine disrupting chemical. Female rats were exposed to vehicle or BPA 25 ng/kg·d, 25 μg/kg·d, or 5 mg/kg·d from postnatal day (PND)1 to PND5 or PND15. Exposure to 25 ng/kg·d of BPA for 5 or 15 days was followed by a delay in developmental reduction of GnRH IPI studied ex vivo on PND20. After 15 days of exposure to that low dose of BPA, vaginal opening tended to be delayed. In contrast, exposure to BPA 5 mg/kg·d for 15 days resulted in a premature reduction in GnRH IPI and a trend toward early vaginal opening. RNA sequencing analysis on PND20 indicated that exposure to BPA resulted in opposing dose effects on the mRNA expression of hypothalamic genes involved in gamma aminobutyric acid A (GABAA) neurotransmission. The study of GnRH secretion in vitro in the presence of GABAA receptor agonist/antagonist confirmed an increased or a reduced GABAergic tone after in vivo exposure to the very low or the high dose of BPA, respectively. Overall, we show for the first time that neonatal exposure to BPA leads to opposing dose-dependent effects on the neuroendocrine control of puberty in the female rat. A very low and environmentally relevant dose of BPA delays neuroendocrine maturation related to puberty through increased inhibitory GABAergic neurotransmission.

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Pubertal Onset in Girls is Strongly Influenced by Genetic Variation Affecting FSH Action

Cited by 30 publications

References 48 publications

Nicotine and the adolescent brain

Nicotine and the adolescent brain

Adaptive capabilities and fitness consequences associated with pollution exposure in fish

Delayed Neuroendocrine Sexual Maturation in Female Rats After a Very Low Dose of Bisphenol A Through Altered GABAergic Neurotransmission and Opposing Effects of a High Dose

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