Linked Life Data

9356023

Source:http://linkedlifedata.com/resource/pubmed/id/9356023

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1997-11-21
pubmed:abstractText
Rats fed a high-fat diet develop skeletal muscle insulin resistance. There is disagreement regarding whether a decrease in the GLUT4 isoform of the glucose transporter is responsible. We found that feeding rats a high-fat diet that reduced the responsiveness of glucose transport to insulin in skeletal muscles by approximately 25-45% in 4 weeks, had no significant effect on muscle GLUT4 content. There is also controversy regarding whether the contraction/anoxia activated pathway of glucose transport stimulation is affected by fat feeding. We found that stimulation of muscle glucose transport by either swimming, in situ contractions, or anoxia was depressed to a similar extent as insulin responsiveness in high-fat-fed rats. It has been suggested that the muscle insulin resistance caused by a high-fat diet is due to increased fat oxidation and glucose-fatty acid cycle activity. However, we found that insulin-stimulated glucose transport was reduced by approximately 40% when muscles of fat-fed rats were incubated under anoxic conditions under which fatty acid oxidation should not occur. Rats maintained on the high-fat diet up to 32 weeks developed the characteristics of the abdominal obesity syndrome, including insulin resistance, hyperinsulinemia, hyperglycemia, elevated LDL cholesterol and VLDL triglycerides, and marked visceral obesity. We conclude that 1) in rats fed a high-fat diet the muscle insulin resistance is not due to a decrease in total GLUT4 content or to increased fat oxidation, 2) fat feeding also results in resistance of muscle glucose transport to stimulation via the contraction/anoxia pathway, and 3) rats fed a high-fat diet may be a useful model of the abdominal obesity syndrome.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1761-7
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:9356023-Adipose Tissue, pubmed-meshheading:9356023-Animals, pubmed-meshheading:9356023-Anoxia, pubmed-meshheading:9356023-Blood Glucose, pubmed-meshheading:9356023-Body Weight, pubmed-meshheading:9356023-Deoxyglucose, pubmed-meshheading:9356023-Dietary Fats, pubmed-meshheading:9356023-Glucose, pubmed-meshheading:9356023-Glucose Transporter Type 4, pubmed-meshheading:9356023-Insulin, pubmed-meshheading:9356023-Insulin Resistance, pubmed-meshheading:9356023-Male, pubmed-meshheading:9356023-Monosaccharide Transport Proteins, pubmed-meshheading:9356023-Muscle, Skeletal, pubmed-meshheading:9356023-Muscle Contraction, pubmed-meshheading:9356023-Muscle Proteins, pubmed-meshheading:9356023-Organ Size, pubmed-meshheading:9356023-Physical Exertion, pubmed-meshheading:9356023-Rats, pubmed-meshheading:9356023-Rats, Wistar, pubmed-meshheading:9356023-Swimming, pubmed-meshheading:9356023-Ulnar Nerve
pubmed:year
1997
pubmed:articleTitle
Insulin resistance of muscle glucose transport in rats fed a high-fat diet: a reevaluation.
pubmed:affiliation
Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't