Document Detail


Skeletal muscle inflammation is not responsible for the rapid impairment in adiponectin response with high-fat feeding in rats.
MedLine Citation:
PMID:  20554937     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Adiponectin (Ad) is an insulin-sensitizing adipokine known to stimulate fatty acid (FA) oxidation in skeletal muscle. Skeletal muscle can become resistant to Ad very rapidly, after only 3 days of high saturated fat feeding in rats. Whether the same occurs following a high polyunsaturated fat diet is unknown. Obesity, insulin resistance, and hyperlipidemia are recognized as low-grade inflammatory diseases; therefore, we hypothesized that high-fat feeding induces inflammation, which interferes with Ad action at skeletal muscle. To this end, rats were placed into one of three dietary groups, control (CON, 10% kcal from fat), high saturated (SAT), or high polyunsaturated (PUFA) fat (60% kcal from fat) for 3 days to determine whether Ad resistance develops. Half of the animals from each group were further supplemented with aspirin, a common anti-inflammatory drug. Ad stimulated FA metabolism, Ad signaling intermediates [AdipoR1, APPL1, LKB1, AMPK, and acetyl-CoA carboxylase (ACC)], and inflammatory proteins [Toll-like receptor (TLR4), IKK alpha/beta, IkappaB alpha, NF-kappaB, suppressor of cytokine signaling-3 (SOCS3), and JNK] were measured in soleus muscle. Three days of SAT feeding induced Ad resistance in soleus muscle, assessed as an inability of Ad to phosphorylate ACC and increase FA oxidation. In PUFA-fed animals, Ad-stimulated FA oxidation and ACC phosphorylation to the same degree as CON animals (FA oxidation: +35%, +41%; pACC +29%, +19%; CON, PUFA, P < 0.05). However, neither SAT nor PUFA feeding for 3 days induced skeletal muscle inflammation. Surprisingly, aspirin prevented Ad-stimulated increases in FA oxidation. In conclusion, FA type is critical in the development of Ad resistance, but this does not appear to be mediated by inflammation.
Authors:
Kerry L Mullen; Justine M Tishinsky; Lindsay E Robinson; David J Dyck
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-06-16
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  299     ISSN:  1522-1490     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-08-03     Completed Date:  2010-09-08     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R500-8     Citation Subset:  IM    
Affiliation:
Dept. of Human Health and Nutritional Sciences, Univ. of Guelph, Ontario, Canada, N1G 2W1.
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MeSH Terms
Descriptor/Qualifier:
Acetyl-CoA Carboxylase / metabolism
Adiponectin / metabolism*
Animals
Anti-Inflammatory Agents, Non-Steroidal / pharmacology
Aspirin / pharmacology
Dietary Fats / administration & dosage,  blood,  metabolism*
Fatty Acids / metabolism
Fatty Acids, Unsaturated / metabolism
Female
Inflammation Mediators / metabolism
Muscle, Skeletal / drug effects,  metabolism*
Myositis / etiology,  metabolism*,  prevention & control
Oxidation-Reduction
Phosphorylation
Rats
Rats, Sprague-Dawley
Time Factors
Grant Support
ID/Acronym/Agency:
//Canadian Institutes of Health Research
Chemical
Reg. No./Substance:
0/Adiponectin; 0/Anti-Inflammatory Agents, Non-Steroidal; 0/Dietary Fats; 0/Fatty Acids; 0/Fatty Acids, Unsaturated; 0/Inflammation Mediators; 50-78-2/Aspirin; EC 6.4.1.2/Acetyl-CoA Carboxylase

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


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