Linked Life Data

10480880

Source:http://linkedlifedata.com/resource/pubmed/id/10480880

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
38
pubmed:dateCreated
1999-10-13
pubmed:abstractText
Increasing evidence has implicated the membrane protein CD36 (FAT) in binding and transport of long chain fatty acids (FA). To determine the physiological role of CD36, we examined effects of its overexpression in muscle, a tissue that depends on FA for its energy needs and is responsible for clearing a major fraction of circulating FA. Mice with CD36 overexpression in muscle were generated using the promoter of the muscle creatine kinase gene (MCK). Transgenic (MCK-CD36) mice had a slightly lower body weight than control litter mates. This reflected a leaner body mass with less overall adipose tissue, as evidenced by magnetic resonance spectroscopy. Soleus muscles from transgenic animals exhibited a greatly enhanced ability to oxidize fatty acids in response to stimulation/contraction. This increased oxidative ability was not associated with significant alterations in histological appearance of muscle fibers. Transgenic mice had lower blood levels of triglycerides and fatty acids and a reduced triglyceride content of very low density lipoproteins. Blood cholesterol levels were slightly lower, but no significant decrease in the cholesterol content of major lipoprotein fractions was measured. Blood glucose was significantly increased, while insulin levels were similar in the fed state and higher in the fasted state. However, glucose tolerance curves, determined at 20 weeks of age, were similar in control and transgenic mice. In summary, the study documented, in vivo, the role of CD36 to facilitate cellular FA uptake. It also illustrated importance of the uptake process in muscle to overall FA metabolism and glucose utilization.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
17
pubmed:volume
274
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
26761-6
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:10480880-Adipose Tissue, pubmed-meshheading:10480880-Animals, pubmed-meshheading:10480880-Antigens, CD36, pubmed-meshheading:10480880-Blood Glucose, pubmed-meshheading:10480880-Body Composition, pubmed-meshheading:10480880-Cholesterol, pubmed-meshheading:10480880-Fatty Acids, pubmed-meshheading:10480880-Female, pubmed-meshheading:10480880-Insulin, pubmed-meshheading:10480880-Magnetic Resonance Spectroscopy, pubmed-meshheading:10480880-Male, pubmed-meshheading:10480880-Membrane Glycoproteins, pubmed-meshheading:10480880-Mice, pubmed-meshheading:10480880-Mice, Transgenic, pubmed-meshheading:10480880-Muscle Contraction, pubmed-meshheading:10480880-Muscles, pubmed-meshheading:10480880-Organic Anion Transporters, pubmed-meshheading:10480880-Oxidation-Reduction, pubmed-meshheading:10480880-Triglycerides
pubmed:year
1999
pubmed:articleTitle
Muscle-specific overexpression of FAT/CD36 enhances fatty acid oxidation by contracting muscle, reduces plasma triglycerides and fatty acids, and increases plasma glucose and insulin.
pubmed:affiliation
Department of Physiology and Biophysics, State University of New York, Stony Brook, New York 11794-8661, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't