Document Detail


High-fat diet results in postprandial insulin resistance that involves parasympathetic dysfunction.
MedLine Citation:
PMID:  20594392     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Different diets have distinct impacts on glucose homoeostasis, for which insulin sensitivity (IS) after a meal (postprandial IS) is highly relevant. Postprandial IS depends upon hepatic parasympathetic activation and glutathione content elevation. We tested the hypothesis that postprandial IS is compromised in high-fat diet (HFD)-induced obesity. Sprague-Dawley rats were fed a standard diet (STD, n 10), 1-week HFD (n 9) or 4-week HFD (n 8). IS was tested in postprandial state using the rapid IS test (RIST) before and after the blockade of the parasympathetic nerves (atropine, 1 mg/kg); parasympathetic-dependent IS was obtained from the difference between control and post-atropine RIST. Fasting IS was also assessed in the STD-fed rats (n 4) and 4-week HFD-fed rats (n 3) using the RIST. Whole-body fat and regional fat pads were heavier in the 1-week HFD-fed rats (79.8 (SE 7.9) and 23.7 (SE 1.0) g, respectively) or 4-week HFD-fed rats (106.5 (SE 6.1) and 30.1 (SE 1.4) g, respectively) than in the STD-fed rats (32.5 (SE 3.7) and 13.7 (SE 1.0) g, respectively; P < 0.001). Fasted-state IS was similar between the groups studied. Postprandial IS was higher in the STD-fed rats (185.8 (SE 5.6) mg glucose/kg body weight (bw)) than in both the 1-week HFD-fed rats (108.8 (SE 2.9) mg glucose/kg bw; P < 0.001) and 4-week HFD-fed rats (69.3 (SE 2.6) mg glucose/kg bw; P < 0.001). Parasympathetic-dependent IS was impaired in both HFD-fed groups (STD, 108.9 (SE 3.9) mg glucose/kg bw; 1-week HFD, 38.6 (SE 4.2) mg glucose/kg bw; 4-week HFD, 5.4 (SE 1.7) mg glucose/kg bw; P < 0.001). Total (postprandial) and parasympathetic-dependent IS correlated negatively with whole-body fat (R² 0.81 and 0.87) and regional adiposity (R² 0.85 and 0.79). In conclusion, fat accumulation induced by HFD is associated with postprandial insulin resistance, but not with fasting insulin resistance. HFD-associated postprandial insulin resistance is largely mediated by impairment of parasympathetic-dependent insulin action, which correlates with adiposity.
Authors:
Ricardo A Afonso; W Wayne Lautt; Josh Schafer; Dallas J Legare; Antonio G Oliveira; M Paula Macedo
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-07-02
Journal Detail:
Title:  The British journal of nutrition     Volume:  104     ISSN:  1475-2662     ISO Abbreviation:  Br. J. Nutr.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-11-10     Completed Date:  2010-12-16     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0372547     Medline TA:  Br J Nutr     Country:  England    
Other Details:
Languages:  eng     Pagination:  1450-9     Citation Subset:  IM    
Affiliation:
Department of Biochemistry, Faculdade de Ciências Médicas (FCM), Universidade Nova de Lisboa (UNL), Campo Martires da Patria, 130, 1169-056 Lisboa, Portugal.
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MeSH Terms
Descriptor/Qualifier:
Animals
Autonomic Nervous System Diseases / chemically induced*
Blood Glucose / drug effects
Blood Pressure / drug effects
Body Weight / drug effects
Dietary Fats / adverse effects*
Glutathione / metabolism
Insulin Resistance / physiology*
Liver / drug effects,  metabolism
Male
Postprandial Period
Rats
Rats, Sprague-Dawley
Grant Support
ID/Acronym/Agency:
//Canadian Institutes of Health Research
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Dietary Fats; 70-18-8/Glutathione

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


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