Document Detail


Sympathetic overactivity precedes metabolic dysfunction in a fructose model of glucose intolerance in mice.
MedLine Citation:
PMID:  22319048     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Consumption of high levels of fructose in humans and animals leads to metabolic and cardiovascular dysfunction. There are questions as to the role of the autonomic changes in the time course of fructose-induced dysfunction. C57/BL male mice were given tap water or fructose water (100 g/l) to drink for up to 2 mo. Groups were control (C), 15-day fructose (F15), and 60-day fructose (F60). Light-dark patterns of arterial pressure (AP) and heart rate (HR), and their respective variabilities were measured. Plasma glucose, lipids, insulin, leptin, resistin, adiponectin, and glucose tolerance were quantified. Fructose increased systolic AP (SAP) at 15 and 60 days during both light (F15: 123 ± 2 and F60: 118 ± 2 mmHg) and dark periods (F15: 136 ± 4 and F60: 136 ± 5 mmHg) compared with controls (light: 111 ± 2 and dark: 117 ± 2 mmHg). SAP variance (VAR) and the low-frequency component (LF) were increased in F15 (>60% and >80%) and F60 (>170% and >140%) compared with C. Cardiac sympatho-vagal balance was enhanced, while baroreflex function was attenuated in fructose groups. Metabolic parameters were unchanged in F15. However, F60 showed significant increases in plasma glucose (26%), cholesterol (44%), triglycerides (22%), insulin (95%), and leptin (63%), as well as glucose intolerance. LF of SAP was positively correlated with SAP. Plasma leptin was correlated with triglycerides, insulin, and glucose tolerance. Results show that increased sympathetic modulation of vessels and heart preceded metabolic dysfunction in fructose-consuming mice. Data suggest that changes in autonomic modulation may be an initiating mechanism underlying the cluster of symptoms associated with cardiometabolic disease.
Authors:
Katia De Angelis; Danielle D Senador; Cristiano Mostarda; Maria C Irigoyen; Mariana Morris
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-02-08
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  302     ISSN:  1522-1490     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2012 Apr 
Date Detail:
Created Date:  2012-04-16     Completed Date:  2012-06-18     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R950-7     Citation Subset:  IM    
Affiliation:
Laboratory of Translational Physiology, Nove de Julho University, São Paulo, Brazil.
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MeSH Terms
Descriptor/Qualifier:
Animals
Baroreflex / drug effects,  physiology
Blood Glucose / metabolism
Blood Pressure / drug effects,  physiology
Body Weight / drug effects,  physiology
Disease Models, Animal
Fructose / adverse effects*
Glucose Intolerance / chemically induced,  metabolism*,  physiopathology
Heart Rate / drug effects,  physiology
Insulin / blood
Insulin Resistance / physiology
Leptin / blood
Lipids / blood
Male
Mice
Sympathetic Nervous System / metabolism,  physiopathology*
Grant Support
ID/Acronym/Agency:
DK59630/DK/NIDDK NIH HHS; R-01-HL-093567/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Insulin; 0/Leptin; 0/Lipids; 30237-26-4/Fructose
Comments/Corrections

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


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