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Endocrine cells produce hormones to communicate with remote target cells found in other organs. The hormone reaches these distant areas using the circulatory system. This exposes the whole organism to the hormone but only those cells expressing hormone receptors or target cells are affected. Thus, endocrine signaling induces slow responses from its target cells but these effects also last longer.
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The endocrine system sends hormones—chemical signals—through the bloodstream to target cells—the cells the hormones selectively affect. These signals are produced in endocrine cells, secreted into the extracellular fluid, and then diffuse into the blood. Eventually, they diffuse out of the blood and bind to target cells which have specialized receptors to recognize the hormones.
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Endocrine disrupters and possible contribution to pubertal changes.

Julie Fudvoye1, David Lopez-Rodriguez2, Delphine Franssen2

  • 1Neuroendocrinology Unit, GIGA Neurosciences, University of Liège, Sart-Tilman, B-4000, Liège, Belgium; Department of Pediatrics, CHU de Liège, Rue de Gaillarmont 600, B-4032, Chênée, Belgium.

Best Practice & Research. Clinical Endocrinology & Metabolism
|August 12, 2019
PubMed
Summary

Environmental pollutants like endocrine disrupting chemicals (EDCs) can alter puberty timing. Early life exposure may lead to reproductive issues, impacting neuroendocrine and peripheral systems.

Keywords:
endocrine disruptorsenvironmentgonadotropin releasing hormonehypothalamuspubertysecular trend

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Area of Science:

  • Reproductive endocrinology
  • Developmental toxicology
  • Environmental health

Background:

  • Puberty onset is influenced by fetal and early postnatal development.
  • Environmental pollutants, particularly endocrine disrupting chemicals (EDCs), pose risks during critical developmental windows.
  • Evidence linking EDCs to altered human pubertal timing is inconclusive, but observed shifts in pubertal sign distribution suggest environmental factors.

Purpose of the Study:

  • To explore the impact of endocrine disrupting chemicals (EDCs) on pubertal timing.
  • To investigate the neuroendocrine and peripheral mechanisms underlying EDC-induced reproductive alterations.
  • To synthesize evidence on the role of early-life exposure to environmental factors in reproductive health.

Main Methods:

  • Review of human epidemiological data on pubertal timing and EDC exposure.
  • Analysis of age distribution patterns of pubertal signs.
  • Synthesis of findings from rodent and ovine studies on fetal and neonatal EDC exposure.
  • Examination of neuroendocrine pathways in the hypothalamus and peripheral reproductive tissues.

Main Results:

  • Human evidence for EDC-induced pubertal timing alterations is equivocal.
  • Pubertal signs show a skewed distribution: earlier for initial stages, later for final stages, suggesting environmental influence.
  • Animal studies confirm that fetal and neonatal EDC exposure can disrupt reproductive programming.
  • Affected mechanisms include hypothalamic neuroendocrine regulation and peripheral effects on gonads and mammary glands.

Conclusions:

  • Early-life exposure to endocrine disrupting chemicals (EDCs) can disrupt pubertal development and have long-term reproductive consequences.
  • The observed shifts in pubertal timing distribution highlight the potential impact of environmental factors.
  • Neuroendocrine and peripheral mechanisms are implicated in EDC-induced reproductive disturbances, supporting the 'early origin of health and disease' concept.