Document Detail


Cardiac and skeletal muscle fatty acid transport and transporters and triacylglycerol and fatty acid oxidation in lean and Zucker diabetic fatty rats.
MedLine Citation:
PMID:  19675275     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We examined fatty acid transporters, transport, and metabolism in hearts and red and white muscles of lean and insulin-resistant (week 6) and type 2 diabetic (week 24) Zucker diabetic fatty (ZDF) rats. Cardiac fatty acid transport was similar in lean and ZDF hearts at week 6 but was reduced at week 24 (-40%) in lean but not ZDF hearts. Red muscle of ZDF rats exhibited an early susceptibility to upregulation (+66%) of fatty acid transport at week 6 that was increased by 50% in lean and ZDF rats at week 24 but remained 44% greater in red muscle of ZDF rats. In white muscle, no differences were observed in fatty acid transport between groups or from week 6 to week 24. In all tissues (heart and red and white muscle), FAT/CD36 protein and plasmalemmal content paralleled the changes in fatty acid transport. Triacylglycerol content in red and white muscles, but not heart, in lean and ZDF rats correlated with fatty acid transport (r = 0.91) and sarcolemmal FAT/CD36 (r = 0.98). Red and white muscle fatty acid oxidation by isolated mitochondria was not impaired in ZDF rats but was reduced by 18-24% in red muscle of lean rats at week 24. Thus, in red, but not white, muscle of insulin-resistant and type 2 diabetic animals, a marked upregulation in fatty acid transport and intramuscular triacylglycerol was associated with increased levels of FAT/CD36 expression and plasmalemmal content. In heart, greater rates of fatty acid transport and FAT/CD36 in ZDF rats (week 24) were attributable to the inhibition of age-related reductions in these parameters. However, intramuscular triacylglycerol did not accumulate in hearts of ZDF rats. Thus insulin resistance and type 2 diabetes are accompanied by tissue-specific differences in FAT/CD36 and fatty acid transport and metabolism. Upregulation of fatty acid transport increased red muscle, but not cardiac, triacylglycerol accumulation. White muscle lipid metabolism dysregulation was not observed.
Authors:
Arend Bonen; Graham P Holloway; Narendra N Tandon; Xiao-Xia Han; Jay McFarlan; Jan F C Glatz; Joost J F P Luiken
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-08-12
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  297     ISSN:  1522-1490     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2009 Oct 
Date Detail:
Created Date:  2009-09-28     Completed Date:  2009-10-13     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:  R1202-12     Citation Subset:  IM    
Affiliation:
Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada. abonen@uoguelph.ca
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, CD36 / metabolism*
Biological Transport
Blood Glucose / metabolism
Citrate (si)-Synthase / metabolism
Diabetes Mellitus, Type 2 / metabolism*,  physiopathology
Disease Models, Animal
Fatty Acids / blood,  metabolism*
Glucose Transporter Type 4 / metabolism
Insulin / blood
Insulin Resistance*
Male
Mitochondria, Muscle / metabolism
Muscle Fibers, Fast-Twitch / metabolism
Muscle Fibers, Slow-Twitch / metabolism
Muscle, Skeletal / metabolism*
Myocardium / metabolism*
Obesity / metabolism*,  physiopathology
Oxidation-Reduction
Rats
Rats, Zucker
Thinness / metabolism*,  physiopathology
Time Factors
Triglycerides / metabolism*
Chemical
Reg. No./Substance:
0/Antigens, CD36; 0/Blood Glucose; 0/Fatty Acids; 0/Glucose Transporter Type 4; 0/Slc2a4 protein, rat; 0/Triglycerides; 11061-68-0/Insulin; EC 2.3.3.1/Citrate (si)-Synthase

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


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