Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
|
| pubmed:dateCreated |
1992-5-22
|
| pubmed:abstractText |
To examine the mechanisms of hyperglycemia-induced insulin resistance, eight insulin-dependent (type I) diabetic men were studied twice, after 24 h of hyperglycemia (mean blood glucose 20.0 +/- 0.3 mM, i.v. glucose) and after 24 h of normoglycemia (7.1 +/- 0.4 mM, saline) while receiving identical diets and insulin doses. Whole-body and forearm glucose uptake were determined during a 300-min insulin infusion (serum free insulin 359 +/- 22 and 373 +/- 29 pM, after hyper- and normoglycemia, respectively). Muscle biopsies were taken before and at the end of the 300-min insulin infusion. Plasma glucose levels were maintained constant during the 300-min period by keeping glucose for 150 min at 16.7 +/- 0.1 mM after 24-h hyperglycemia and increasing it to 16.5 +/- 0.1 mM after normoglycemia and by allowing it thereafter to decrease in both studies to normoglycemia. During the normoglycemic period (240-300 min), total glucose uptake (25.0 +/- 2.8 vs. 33.8 +/- 3.9 mumol.kg-1 body wt.min-1, P less than 0.05) was 26% lower, forearm glucose uptake (11 +/- 4 vs. 18 +/- 3 mumol.kg-1 forearm.min-1, P less than 0.05) was 35% lower, and nonoxidative glucose disposal (8.9 +/- 2.2 vs. 19.4 +/- 3.3 mumol.kg-1 body wt-1min-1, P less than 0.01) was 54% lower after 24 h of hyper- and normoglycemia, respectively. Glucose oxidation rates were similar. Basal muscle glycogen content was similar after 24 h of hyperglycemia (234 +/- 23 mmol/kg dry muscle) and normoglycemia (238 +/- 22 mmol/kg dry muscle). Insulin increased muscle glycogen to 273 +/- 22 mmol/kg dry muscle after 24 h of hyperglycemia and to 296 +/- 33 mmol/kg dry muscle after normoglycemia (P less than 0.05 vs. 0 min for both). Muscle ATP, free glucose, glucose-6-phosphate, and fructose-6-phosphate concentrations were similar after both 24-h treatment periods and did not change in response to insulin. We conclude that a marked decrease in whole-body, muscle, and nonoxidative glucose disposal can be induced by hyperglycemia alone.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Blood Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Fatty Acids, Nonesterified,
http://linkedlifedata.com/resource/pubmed/chemical/Fructosephosphates,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose-6-Phosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Glucosephosphates,
http://linkedlifedata.com/resource/pubmed/chemical/Glycogen,
http://linkedlifedata.com/resource/pubmed/chemical/Growth Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Hydrocortisone,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Lactates,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium,
http://linkedlifedata.com/resource/pubmed/chemical/Serum Albumin,
http://linkedlifedata.com/resource/pubmed/chemical/fructose-6-phosphate
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
May
|
| pubmed:issn |
0012-1797
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
41
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
571-80
|
| pubmed:dateRevised |
2011-11-17
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| pubmed:meshHeading |
pubmed-meshheading:1568526-Adenosine Triphosphate,
pubmed-meshheading:1568526-Adult,
pubmed-meshheading:1568526-Biopsy,
pubmed-meshheading:1568526-Blood Glucose,
pubmed-meshheading:1568526-Circadian Rhythm,
pubmed-meshheading:1568526-Diabetes Mellitus, Type 1,
pubmed-meshheading:1568526-Energy Metabolism,
pubmed-meshheading:1568526-Fatty Acids, Nonesterified,
pubmed-meshheading:1568526-Fructosephosphates,
pubmed-meshheading:1568526-Glucose-6-Phosphate,
pubmed-meshheading:1568526-Glucosephosphates,
pubmed-meshheading:1568526-Glycogen,
pubmed-meshheading:1568526-Growth Hormone,
pubmed-meshheading:1568526-Humans,
pubmed-meshheading:1568526-Hydrocortisone,
pubmed-meshheading:1568526-Hyperglycemia,
pubmed-meshheading:1568526-Insulin,
pubmed-meshheading:1568526-Insulin Resistance,
pubmed-meshheading:1568526-Lactates,
pubmed-meshheading:1568526-Male,
pubmed-meshheading:1568526-Muscles,
pubmed-meshheading:1568526-Osmolar Concentration,
pubmed-meshheading:1568526-Oxidation-Reduction,
pubmed-meshheading:1568526-Potassium,
pubmed-meshheading:1568526-Serum Albumin
|
| pubmed:year |
1992
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| pubmed:articleTitle |
Mechanisms of hyperglycemia-induced insulin resistance in whole body and skeletal muscle of type I diabetic patients.
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| pubmed:affiliation |
Second Department of Medicine, University of Helsinki, Finland.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|