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Chronic stress, visceral obesity and gonadal dysfunction
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Kyrou, Ioannis and Tsigos, Constantine (2008) Chronic stress, visceral obesity and gonadal dysfunction. Hormones, Vol.7 (No.4). pp. 287-293.
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Abstract
Chronic stress represents a prolonged state of dyshomeostasis caused by intense and frequently imposed stressors. Obesity constitutes a chronic dysmetabolic state, leading progressively to a spectrum of metabolic complications, such as diabetes, dyslipidemia, hypertension and cardiovascular disease. A growing body of evidence supports the existence of significant interactions between stress and obesity, with chronic stress promoting weight gain, and consequently excessive fat accumulation especially visceral, all these factors contributing to the development of a chronic stressful state. Maintaining body homeostasis is a prerequisite for normal reproductive function, which is vital for the survival of the species and an important process of natural selection. Under chronic stress, reproductive function is suspended and disrupted due to central and peripheral actions of hormones, adipokines and pro-inflammatory cytokines that inhibit the activity of the hypothalamic-pituitary gonadal (HPG) axis at various levels. Clinical and experimental data link both obesity and chronic stress to dysregulation of the gonadal axis, via independent and synergistic mechanisms, which may chronically lead to reproductive dysfunction and reduced fertility.
Item Type: | Journal Item | ||||
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Subjects: | R Medicine > RC Internal medicine | ||||
Divisions: | Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School | ||||
Journal or Publication Title: | Hormones | ||||
Publisher: | Hellenic Endocrine Society | ||||
ISSN: | 1109-3099 | ||||
Official Date: | October 2008 | ||||
Dates: |
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Volume: | Vol.7 | ||||
Number: | No.4 | ||||
Number of Pages: | 7 | ||||
Page Range: | pp. 287-293 | ||||
Status: | Not Peer Reviewed | ||||
Publication Status: | Published | ||||
Access rights to Published version: | Restricted or Subscription Access |
Data sourced from Thomson Reuters' Web of Knowledge
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