Document Detail

The role of endocrine counterregulation for estimating insulin sensitivity from intravenous glucose tolerance tests.
MedLine Citation:
PMID:  16595595     Owner:  NLM     Status:  MEDLINE    
CONTEXT: During insulin-modified frequently sampled iv glucose tolerance tests (IM-FSIGT), which allow assessment of insulin action, plasma glucose can markedly decrease. OBJECTIVE: This study aimed to assess the counterregulatory impact of the insulin-induced fall of glucose on minimal model-derived indices of insulin sensitivity (S(I)) and glucose effectiveness. PARTICIPANTS: Thirteen nondiabetic volunteers (seven males, six females, aged 26 +/- 1 yr, body mass index 22.1 +/- 0.7 kg/m(2)) were studied. DESIGN: All participants were studied in random order during IM-FSIGT (0.3 g/kg glucose; 0.03 U/kg insulin at 20 min) and during identical conditions but with a variable glucose infusion preventing a decrease of plasma glucose concentration below euglycemia (IM-FSIGT-CLAMP). Five participants additionally underwent euglycemic-hyperinsulinemic (1 clamp tests. RESULTS: Plasma glucose declined during IM-FSIGT to its nadir of 50 +/- 3 mg/dl at 60 min in parallel to a rise (P < 0.05 vs. basal) of plasma glucagon, cortisol, epinephrine, and GH. Glucose infusion rates of 4.6 +/- 0.5 between 30 and 180 min during IM-FSIGT-CLAMP prevented the decline of plasma glucose and the hypoglycemia counterregulatory hormone response. S(I) was approximately 68% lower during IM-FSIGT (3.40 +/- 0.36 vs. IM-FSIGT-CLAMP: 10.71 +/- 1.06 10(-4).min(-1) per microU/ml, P < 0.0001), whereas glucose effectiveness did not differ between both protocols (0.024 +/- 0.002 vs. 0.021 +/- 0.003 min(-1), P = NS). Compared with the euglycemic hyperinsulinemic clamp test, S(I) expressed in identical units from IM-FSIGT was approximately 66% (P < 0.001) lower but did not differ between the euglycemic hyperinsulinemic clamp test and the IM-FSIGT-CLAMP (P = NS). CONCLUSIONS: The transient fall of plasma glucose during IM-FSIGT results in lower estimates of S(I), which can be explained by hormonal response to hypoglycemia.
Attila Brehm; Karl Thomaseth; Elisabeth Bernroider; Peter Nowotny; Werner Waldhäusl; Giovanni Pacini; Michael Roden
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-04-04
Journal Detail:
Title:  The Journal of clinical endocrinology and metabolism     Volume:  91     ISSN:  0021-972X     ISO Abbreviation:  J. Clin. Endocrinol. Metab.     Publication Date:  2006 Jun 
Date Detail:
Created Date:  2006-06-07     Completed Date:  2006-06-29     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0375362     Medline TA:  J Clin Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2272-8     Citation Subset:  AIM; IM    
Division of Endocrinology and Metabolism, Department of Internal Medicine 3, Medical University of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria.
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MeSH Terms
Blood Glucose / analysis*
Fatty Acids, Nonesterified / blood
Glucagon / blood
Glucose Clamp Technique
Glucose Tolerance Test*
Hydrocortisone / blood
Insulin / blood,  pharmacology*
Norepinephrine / blood
Reg. No./Substance:
0/Blood Glucose; 0/Fatty Acids, Nonesterified; 11061-68-0/Insulin; 50-23-7/Hydrocortisone; 51-41-2/Norepinephrine; 9007-92-5/Glucagon

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

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