Document Detail


Hypothalamic nitric oxide in hypoglycemia detection and counterregulation: a two-edged sword.
MedLine Citation:
PMID:  20518706     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hypoglycemia is the main complication for patients with type 1 diabetes mellitus receiving intensive insulin therapy. In addition to the obvious deleterious effects of acute hypoglycemia on brain function, recurrent episodes of hypoglycemia (RH) have an even more insidious effect. RH impairs the ability of the brain to detect and initiate an appropriate counterregulatory response (CRR) to restore euglycemia in response to subsequent hypoglycemia. Knowledge of mechanisms involved in hypoglycemia detection and counterregulation has significantly improved over the past 20 years. Glucose sensitive neurons (GSNs) in the ventromedial hypothalamus (VMH) may play a key role in the CRR. VMH nitric oxide (NO) production has recently been shown to be critical for both the CRR and glucose sensing by glucose-inhibited neurons. Interestingly, downstream effects of NO may also contribute to the impaired CRR after RH. In this review, we will discuss current literature regarding the molecular mechanisms by which VMH GSNs sense glucose. Putative roles of GSNs in the detection and initiation of the CRR will then be described. Finally, hypothetical mechanisms by which VMH NO production may both facilitate and subsequently impair the CRR will be discussed.
Authors:
Xavier Fioramonti; Zhentao Song; Reema P Vazirani; Annie Beuve; Vanessa H Routh
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2010-08-17
Journal Detail:
Title:  Antioxidants & redox signaling     Volume:  14     ISSN:  1557-7716     ISO Abbreviation:  Antioxid. Redox Signal.     Publication Date:  2011 Feb 
Date Detail:
Created Date:  2011-01-05     Completed Date:  2011-04-14     Revised Date:  2012-02-01    
Medline Journal Info:
Nlm Unique ID:  100888899     Medline TA:  Antioxid Redox Signal     Country:  United States    
Other Details:
Languages:  eng     Pagination:  505-17     Citation Subset:  IM    
Affiliation:
Department of Pharmacology and Physiology, New Jersey Medical School, Newark, New Jersey 07101-1709, USA. fioramxa@umdnj.edu
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MeSH Terms
Descriptor/Qualifier:
Blood Glucose / metabolism
Diabetes Mellitus, Type 1 / drug therapy,  physiopathology
Humans
Hypoglycemia / metabolism*,  physiopathology*
Insulin / therapeutic use
Neurons / metabolism
Nitric Oxide / metabolism*
Nitric Oxide Synthase / metabolism
Signal Transduction / physiology
Ventromedial Hypothalamic Nucleus / cytology,  metabolism*
Grant Support
ID/Acronym/Agency:
1R01DK81358/DK/NIDDK NIH HHS; 2R01DK55619/DK/NIDDK NIH HHS; R01 DK081538-03/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Insulin; 10102-43-9/Nitric Oxide; EC 1.14.13.39/Nitric Oxide Synthase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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