title: Contribution of postprandial insulin and glucose to glucose disposal in normal and insulin-resistant obese subjects.
abstract: We recently found that postprandial hyperinsulinemia does not compensate for the insulin resistance of obese subjects and proposed that postprandial hyperglycemia might be more important in promoting glucose disposal via the mass action effect of glucose. To test this idea we perform oral glucose tolerance tests (OGTT) in six lean and eight obese subjects, measuring glucose and insulin levels. Afterward two insulin infusion studies were performed. During infusion study I, insulin was infused in a dynamic square wave fashion to mimic the individual post-OGTT insulin levels at content euglycemic glucose levels. During study II, glucose and insulin infusions were varied to mimic post-OGTT levels in each subject. Overall glucose turnover was measured isotopically by infusion of [3-3H] glucose. During the OGTT the obese subjects exhibited significantly higher insulin (P less than 0.005) and glucose levels (P less than 0.002). Insulin-stimulated glucose disposal rates and total incremental glucose disposal (IGD) over 4 h during study I at euglycemia were significantly lower in obese compared to lean subjects (area under the curve, 824 +/- 166 vs. 1222 +/- 161 mmol/L.m2; P less than 0.01) despite higher post-OGTT insulin levels in obese subjects. When insulin plus glucose levels were matched to the individual OGTT levels, IGD was not significantly different between obese and control subjects (1712 +/- 253 vs. 1617 +/- 444 mmol/L.m2; P = NS). A significant inverse correlation (r = -0.73; P less than 0.05) existed between the degree of glucose intolerance (OGTT) and the decrease in IGD during the phasic hyperinsulinemic euglycemic study (infusion study I). These data suggest that with increasing insulin resistance, hyperinsulinemia is less effective in compensating for this decrease in insulin action, and hyperglycemia becomes more important in augmenting overall glucose disposal values.
authors.affiliation: Department of Medicine II, University of Vienna, Austria.
authors.forename: R
authors.initials: R
authors.lastname: Klauser
authors.forename: R
authors.initials: R
authors.lastname: Prager
authors.forename: G
authors.initials: G
authors.lastname: Schernthaner
authors.forename: J M
authors.initials: JM
authors.lastname: Olefsky
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D004435:Eating / Q000502:physiology*; D005260:Female; D005947:Glucose / Q000378:metabolism* / Q000502:physiology; D005951:Glucose Tolerance Test; D006801:Humans; D006943:Hyperglycemia / Q000097:blood / Q000378:metabolism / Q000503:physiopathology; D007328:Insulin / Q000097:blood / Q000378:metabolism* / Q000502:physiology; D007333:Insulin Resistance / Q000502:physiology*; D008297:Male; D009765:Obesity / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D001786:Blood Glucose; D007328:Insulin; D005947:Glucose