Document Detail


Role of leptin and central nervous system melanocortins in obesity hypertension.
MedLine Citation:
PMID:  23299052     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE OF REVIEW: Obesity is a major worldwide health problem. Excess weight gain is the most significant preventable cause of increased blood pressure (BP) in patients with essential hypertension and increases the risk for cardiovascular and renal diseases. Our goal is to review the mechanisms that link obesity with hypertension, with special emphasis on the role of leptin and the brain melanocortin system in driving sympathetic activation in obesity.
RECENT FINDINGS: Despite increased interest in obesity as a major risk for developing hypertension, the precise mechanisms linking excess weight gain with increases in BP are still elusive. Current evidence suggests that increased sympathetic nervous system (SNS) activity contributes to impaired renal-pressure natriuresis and sodium retention in obesity. Recent findings indicate that the adipocyte-derived hormone, leptin, activates brain centers that regulate SNS activity through a melanocortin-system-dependent pathway. The interaction of leptin and the brain melanocortin system represents an important area of research to further our understanding of the mechanisms leading to sympathetic activation in obesity.
SUMMARY: Sympathetic overactivity is an important link between excess weight gain and increased BP. Hormones and cytokines secreted by the adipose tissue that interact with neural pathways (e.g. melanocortin system) appear to play a key role in contributing to sympathetic activation in obesity and represent potential new targets for therapies.
Authors:
Alexandre A da Silva; Jussara M do Carmo; John E Hall
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Current opinion in nephrology and hypertension     Volume:  22     ISSN:  1473-6543     ISO Abbreviation:  Curr. Opin. Nephrol. Hypertens.     Publication Date:  2013 Mar 
Date Detail:
Created Date:  2013-02-04     Completed Date:  2013-07-26     Revised Date:  2014-03-07    
Medline Journal Info:
Nlm Unique ID:  9303753     Medline TA:  Curr Opin Nephrol Hypertens     Country:  England    
Other Details:
Languages:  eng     Pagination:  135-40     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Adipocytes / metabolism*
Animals
Blood Pressure
Central Nervous System / metabolism*,  physiopathology
Humans
Hypertension / etiology*,  metabolism,  physiopathology
Leptin / metabolism*
Melanocortins / metabolism*
Obesity / complications*,  metabolism,  physiopathology
Receptor, Melanocortin, Type 4 / metabolism
Signal Transduction
Sympathetic Nervous System / metabolism,  physiopathology
Weight Gain
Grant Support
ID/Acronym/Agency:
P01 HL 51971/HL/NHLBI NIH HHS; P01 HL051971/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Leptin; 0/Melanocortins; 0/Receptor, Melanocortin, Type 4
Comments/Corrections

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