| High-fat diet results in postprandial insulin resistance that involves parasympathetic dysfunction. | |
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MedLine Citation:
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PMID: 20594392 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Ricardo A Afonso; W Wayne Lautt; Josh Schafer; Dallas J Legare; Antonio G Oliveira; M Paula Macedo |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-07-02 |
Journal Detail:
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Title: The British journal of nutrition Volume: 104 ISSN: 1475-2662 ISO Abbreviation: Br. J. Nutr. Publication Date: 2010 Nov |
Date Detail:
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Created Date: 2010-11-10 Completed Date: 2010-12-16 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0372547 Medline TA: Br J Nutr Country: England |
Other Details:
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Languages: eng Pagination: 1450-9 Citation Subset: IM |
Affiliation:
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Department of Biochemistry, Faculdade de Ciências Médicas (FCM), Universidade Nova de Lisboa (UNL), Campo Martires da Patria, 130, 1169-056 Lisboa, Portugal. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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//Canadian Institutes of Health Research |
| Chemical | |
Reg. No./Substance:
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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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