Document Detail

Obesity and adipokines: effects on sympathetic overactivity.
MedLine Citation:
PMID:  22351630     Owner:  NLM     Status:  MEDLINE    
Excess body weight is a major risk factor for cardiovascular disease, increasing the risk of hypertension, hyperglycaemia and dyslipidaemia, recognized as the metabolic syndrome. Adipose tissue acts as an endocrine organ by producing various signalling cytokines called adipokines (including leptin, free fatty acids, tumour necrosis factor-α, interleukin-6, C-reactive protein, angiotensinogen and adiponectin). A chronic dysregulation of certain adipokines can have deleterious effects on insulin signalling. Chronic sympathetic overactivity is also known to be present in central obesity, and recent findings demonstrate the consequence of an elevated sympathetic outflow to organs such as the heart, kidneys and blood vessels. Chronic sympathetic nervous system overactivity can also contribute to a further decline of insulin sensitivity, creating a vicious cycle that may contribute to the development of the metabolic syndrome and hypertension. The cause of this overactivity is not clear, but may be driven by certain adipokines. The purpose of this review is to summarize how obesity, notably central or visceral as observed in the metabolic syndrome, leads to adipokine expression contributing to changes in insulin sensitivity and overactivity of the sympathetic nervous system.
Michael M Smith; Christopher T Minson
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2012-02-20
Journal Detail:
Title:  The Journal of physiology     Volume:  590     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2012 Apr 
Date Detail:
Created Date:  2012-04-25     Completed Date:  2012-11-07     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1787-801     Citation Subset:  IM    
Department of Human Physiology, University of Oregon, Eugene, OR 97403-1240, USA.
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MeSH Terms
Adipokines / metabolism*
Insulin Resistance / physiology
Metabolic Syndrome X / metabolism
Obesity / metabolism*
Sympathetic Nervous System / metabolism*
Grant Support
Reg. No./Substance:

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