|
rdf:type |
|
|
lifeskim:mentions |
umls-concept:C0003402,
umls-concept:C0011142,
umls-concept:C0011860,
umls-concept:C0021655,
umls-concept:C0030705,
umls-concept:C0035696,
umls-concept:C0256926,
umls-concept:C0332120,
umls-concept:C0332281,
umls-concept:C0332307,
umls-concept:C0392756,
umls-concept:C0442117,
umls-concept:C0538674
|
|
pubmed:issue |
9
|
|
pubmed:dateCreated |
2003-8-27
|
|
pubmed:abstractText |
To examine whether genes associated with cellular defense against oxidative stress are associated with insulin sensitivity, patients with type 2 diabetes (n = 7) and age-matched (n = 5) and young (n = 9) control subjects underwent a euglycemic-hyperinsulinemic clamp for 120 min. Muscle samples were obtained before and after the clamp and analyzed for heat shock protein (HSP)72 and heme oxygenase (HO)-1 mRNA, intramuscular triglyceride content, and the maximal activities of beta-hydroxyacyl-CoA dehydrogenase (beta-HAD) and citrate synthase (CS). Basal expression of both HSP72 and HO-1 mRNA were lower (P < 0.05) by 33 and 55%, respectively, when comparing diabetic patients with age-matched and young control subjects, with no differences between the latter groups. Both basal HSP72 (r = 0.75, P < 0.001) and HO-1 (r = 0.50, P < 0.05) mRNA expression correlated with the glucose infusion rate during the clamp. Significant correlations were also observed between HSP72 mRNA and both beta-HAD (r = 0.61, P < 0.01) and CS (r = 0.65, P < 0.01). HSP72 mRNA was induced (P < 0.05) by the clamp in all groups. Although HO-1 mRNA was unaffected by the clamp in both the young and age-matched control subjects, it was increased (P < 0.05) approximately 70-fold in the diabetic patients after the clamp. These data demonstrate that genes involved in providing cellular protection against oxidative stress are defective in patients with type 2 diabetes and correlate with insulin-stimulated glucose disposal and markers of muscle oxidative capacity. The data provide new evidence that the pathogenesis of type 2 diabetes involves perturbations to the antioxidant defense mechanism within skeletal muscle.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
AIM
|
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antioxidants,
http://linkedlifedata.com/resource/pubmed/chemical/Biological Markers,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose Transporter Type 4,
http://linkedlifedata.com/resource/pubmed/chemical/HMOX1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/HSP72 Heat-Shock Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Heat-Shock Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Heme Oxygenase (Decyclizing),
http://linkedlifedata.com/resource/pubmed/chemical/Heme Oxygenase-1,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Monosaccharide Transport Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Muscle Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Peroxidase,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cytoplasmic and Nuclear,
http://linkedlifedata.com/resource/pubmed/chemical/SLC2A4 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Triglycerides
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Sep
|
|
pubmed:issn |
0012-1797
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:volume |
52
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
2338-45
|
|
pubmed:dateRevised |
2011-11-17
|
|
pubmed:meshHeading |
pubmed-meshheading:12941774-Adult,
pubmed-meshheading:12941774-Antioxidants,
pubmed-meshheading:12941774-Biological Markers,
pubmed-meshheading:12941774-Diabetes Mellitus, Type 2,
pubmed-meshheading:12941774-Gene Expression,
pubmed-meshheading:12941774-Glucose Clamp Technique,
pubmed-meshheading:12941774-Glucose Transporter Type 4,
pubmed-meshheading:12941774-HSP72 Heat-Shock Proteins,
pubmed-meshheading:12941774-Heat-Shock Proteins,
pubmed-meshheading:12941774-Heme Oxygenase (Decyclizing),
pubmed-meshheading:12941774-Heme Oxygenase-1,
pubmed-meshheading:12941774-Humans,
pubmed-meshheading:12941774-Insulin,
pubmed-meshheading:12941774-Insulin Resistance,
pubmed-meshheading:12941774-Membrane Proteins,
pubmed-meshheading:12941774-Middle Aged,
pubmed-meshheading:12941774-Monosaccharide Transport Proteins,
pubmed-meshheading:12941774-Muscle, Skeletal,
pubmed-meshheading:12941774-Muscle Proteins,
pubmed-meshheading:12941774-Oxidation-Reduction,
pubmed-meshheading:12941774-Peroxidase,
pubmed-meshheading:12941774-RNA, Messenger,
pubmed-meshheading:12941774-Receptors, Cytoplasmic and Nuclear,
pubmed-meshheading:12941774-Transcription Factors,
pubmed-meshheading:12941774-Triglycerides
|
|
pubmed:year |
2003
|
|
pubmed:articleTitle |
Intramuscular heat shock protein 72 and heme oxygenase-1 mRNA are reduced in patients with type 2 diabetes: evidence that insulin resistance is associated with a disturbed antioxidant defense mechanism.
|
|
pubmed:affiliation |
Exercise Metabolism Group, School of Medical Sciences, RMIT University, Bundoora, Victoria, Australia.
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|
