Source:http://linkedlifedata.com/resource/pubmed/id/17925453
Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
|
| pubmed:dateCreated |
2007-12-10
|
| pubmed:abstractText |
In vivo calorie restriction [CR; consuming 60% of ad libitum (AL) intake] induces elevated insulin-stimulated glucose transport (GT) in skeletal muscle. The mechanisms triggering this adaptation are unknown. The aim of this study was to determine whether physiological reductions in extracellular glucose and/or insulin, similar to those found with in vivo CR, were sufficient to elevate GT in isolated muscles. Epitrochlearis muscles dissected from rats were incubated for 24 h in media with glucose (8 mM) and insulin (80 microU/ml) at levels similar to plasma values of AL-fed rats and compared with muscles incubated with glucose (5.5 mM) and/or insulin (20 microU/ml) at levels similar to plasma values of CR rats. Muscles incubated with CR levels of glucose and insulin for 24 h had a subsequently greater (P < 0.005) GT with 80 microU/ml insulin and 8 mM [(3)H]-3-O-methylglucose but unchanged GT without insulin. Reducing only glucose or insulin for 24 h or both glucose and insulin for 6 h did not induce altered GT. Increased GT after 24-h incubation with CR levels of glucose and insulin was not attributable to increased insulin receptor tyrosine phosphorylation, Akt serine phosphorylation, or Akt substrate of 160 kDa phosphorylation. Nor did 24-h incubation with CR levels of glucose and insulin alter the abundance of insulin receptor, insulin receptor substrate-1, GLUT1, or GLUT4 proteins. These results provide the proof of principle that reductions in extracellular glucose and insulin, similar to in vivo CR, are sufficient to induce an increase in insulin-stimulated glucose transport comparable to the increase found with in vivo CR.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/3-O-Methylglucose,
http://linkedlifedata.com/resource/pubmed/chemical/Adaptor Proteins, Signal Transducing,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose Transporter Type 1,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose Transporter Type 4,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin Receptor Substrate Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Irs1 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Slc2a4 protein, rat
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Dec
|
| pubmed:issn |
0193-1849
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
293
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
E1782-8
|
| pubmed:dateRevised |
2011-11-17
|
| pubmed:meshHeading |
pubmed-meshheading:17925453-3-O-Methylglucose,
pubmed-meshheading:17925453-Adaptor Proteins, Signal Transducing,
pubmed-meshheading:17925453-Animals,
pubmed-meshheading:17925453-Biological Transport,
pubmed-meshheading:17925453-Caloric Restriction,
pubmed-meshheading:17925453-Female,
pubmed-meshheading:17925453-Glucose,
pubmed-meshheading:17925453-Glucose Transporter Type 1,
pubmed-meshheading:17925453-Glucose Transporter Type 4,
pubmed-meshheading:17925453-Insulin,
pubmed-meshheading:17925453-Insulin Receptor Substrate Proteins,
pubmed-meshheading:17925453-Muscle, Skeletal,
pubmed-meshheading:17925453-Phosphorylation,
pubmed-meshheading:17925453-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:17925453-Rats,
pubmed-meshheading:17925453-Rats, Inbred F344,
pubmed-meshheading:17925453-Receptor, Insulin
|
| pubmed:year |
2007
|
| pubmed:articleTitle |
In vitro simulation of calorie restriction-induced decline in glucose and insulin leads to increased insulin-stimulated glucose transport in rat skeletal muscle.
|
| pubmed:affiliation |
Division of Kinesiology, Univ. of Michigan, 401 Washtenaw Ave., Ann Arbor, MI 48109, USA. edarias@umich.edu
|
| pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
|