Journal
JOURNAL OF NEUROENDOCRINOLOGY
Volume 26, Issue 9, Pages 603-612Publisher
WILEY
DOI: 10.1111/jne.12144
Keywords
melatonin; circadian; reproduction; clock gene; mouse; rat
Categories
Funding
- FONDECYT [1110220]
- CONICYT, Chile [ACT1116]
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)
- Conselho Nacional de Desenvolvimento Tecnologico e Cientifico (CNPq
- Brazil)
- Pro-Reitoria de Pesquisa Universidade Federal de Minas Gerais, Brazil
- CONICYT (Chile) [21120472]
- NIEHS - Pilot Grant from the Department of Environmental Medicine at the University of Rochester School of Medicine
- Direct For Biological Sciences
- Division Of Integrative Organismal Systems [1328157] Funding Source: National Science Foundation
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Internal temporal organisation properly synchronised to the environment is crucial for health maintenance. This organisation is provided at the cellular level by the molecular clock, a macromolecular transcription-based oscillator formed by the clock and the clock-controlled genes that is present in both central and peripheral tissues. In mammals, melanopsin in light-sensitive retinal ganglion cells plays a considerable role in the synchronisation of the circadian timing system to the daily light/dark cycle. Melatonin, a hormone synthesised in the pineal gland exclusively at night and an output of the central clock, has a fundamental role in regulating/timing several physiological functions, including glucose homeostasis, insulin secretion and energy metabolism. As such, metabolism is severely impaired after a reduction in melatonin production. Furthermore, light pollution during the night and shift work schedules can abrogate melatonin synthesis and impair homeostasis. Chronodisruption during pregnancy has deleterious effects on the health of progeny, including metabolic, cardiovascular and cognitive dysfunction. Developmental programming by steroids or steroid-mimetic compounds also produces internal circadian disorganisation that may be a significant factor in the aetiology of fertility disorders such as polycystic ovary syndrome. Thus, both early and late in life, pernicious alterations of the endogenous temporal order by environmental factors can disrupt the homeostatic function of the circadian timing system, leading to pathophysiology and/or disease.
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