Document Detail


Estimations of muscle interstitial insulin, glucose, and lactate in type 2 diabetic subjects.
MedLine Citation:
PMID:  11052965     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Previous measurement of insulin in human muscle has shown that interstitial muscle insulin and glucose concentrations are approximately 30-50% lower than in plasma during hyperinsulinemia in normal subjects. The aims of this study were to measure interstitial muscle insulin and glucose in patients with type 2 diabetes to evaluate whether transcapillary transport is part of the peripheral insulin resistance. Ten patients with type 2 diabetes and ten healthy controls matched for sex, age, and body mass index were investigated. Plasma and interstitial insulin, glucose, and lactate (measured by intramuscular in situ-calibrated microdialysis) in the medial quadriceps femoris muscle were analyzed during a hyperinsulinemic euglycemic clamp. Blood flow in the contralateral calf was measured by vein plethysmography. At steady-state clamping, at 60-120 min, the interstitial insulin concentration was significantly lower than arterial insulin in both groups (409 +/- 86 vs. 1,071 +/- 99 pmol/l, P < 0.05, in controls and 584 +/- 165 vs. 1, 253 +/- 82 pmol/l, P < 0.05, in diabetic subjects, respectively). Interstitial insulin concentrations did not differ significantly between diabetic subjects and controls. Leg blood flow was significantly higher in controls (8.1 +/- 1.2 vs. 4.4 +/- 0.7 ml. 100 g(-1).min(-1) in diabetics, P < 0.05). Calculated glucose uptake was less in diabetic patients compared with controls (7.0 +/- 1.2 vs. 10.8 +/- 1.2 micromol. 100 g(-1).min(-1), P < 0.05, respectively). Arterial and interstitial lactate concentrations were both higher in the control group (1.7 +/- 0.1 vs. 1.2 +/- 0.1, P < 0. 01, and 1.8 +/- 0.1 vs. 1.2 +/- 0.2 mmol/l, P < 0.05, in controls and diabetics, respectively). We conclude that, during hyperinsulinemia, muscle interstitial insulin and glucose concentrations did not differ between patients with type 2 diabetes and healthy controls despite a significantly lower leg blood flow in diabetic subjects. It is suggested that decreased glucose uptake in type 2 diabetes is caused by insulin resistance at the cellular level rather than by a deficient access of insulin and glucose surrounding the muscle cell.
Authors:
M Sjöstrand; A Holmäng; L Strindberg; P Lönnroth
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  279     ISSN:  0193-1849     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2000 Nov 
Date Detail:
Created Date:  2000-11-02     Completed Date:  2000-11-09     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  E1097-103     Citation Subset:  IM    
Affiliation:
Lundberg Laboratory for Diabetes Research, Sahlgrenska University Hospital, S-413 45 Goteborg, Sweden. mikaela.sjostrand@medic.gu.se
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MeSH Terms
Descriptor/Qualifier:
Adult
Arteries
Blood Flow Velocity
Blood Glucose / analysis
Body Mass Index
Diabetes Mellitus, Type 2 / metabolism*
Extracellular Space / chemistry
Female
Glucose / analysis*
Glucose Clamp Technique
Humans
Hyperinsulinism
Insulin / analysis*,  blood
Insulin Resistance
Lactic Acid / analysis*,  blood
Leg
Male
Microdialysis
Middle Aged
Muscle, Skeletal / blood supply,  chemistry*
Chemical
Reg. No./Substance:
0/Blood Glucose; 11061-68-0/Insulin; 50-21-5/Lactic Acid; 50-99-7/Glucose

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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