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This Article Full Text Full Text (PDF) All Versions of this Article: 297/2/E532    most recent 00127.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Bonuccelli, S. Articles by Ferrannini, E. PubMed PubMed Citation Articles by Bonuccelli, S. Articles by Ferrannini, E.

Improved tolerance to sequential glucose loading (Staub-Traugott effect): size and mechanisms

¹Department of Internal Medicine, University of Pisa School of Medicine, Pisa; ²Consiglio Nazionale delle Ricerche Institute of Clinical Physiology, Pisa, Italy; ³Department of Biomedical Sciences, the Panum Institute, Copenhagen, Denmark; and ⁴Consiglio Nazionale delle Ricerche, Institute of Biomedical Engineering, Padua, Italy

Submitted 25 February 2009 ; accepted in final form 8 June 2009

Improved glucose tolerance to sequential glucose loading (Staub-Traugott effect) is an important determinant of day-to-day glycemic exposure. Its mechanisms have not been clearly established. We recruited 17 healthy volunteers to receive two sequential oral glucose tolerance tests (OGTTs), at time 0 min and 180 min (Study I). The protocol was repeated on a separate day (Study II) except that plasma glucose was clamped at 8.3 mmol/l between 60 and 180 min. β-Cell function was analyzed by mathematical modeling of C-peptide concentrations. In a subgroup, glucose kinetics were measured by a triple-tracer technique (infusion of [6,6-²H₂]glucose and labeling of the 2 glucose loads with [1-²H]glucose and [U-¹³C]glucose). In both Studies I and II, the plasma glucose response to the second OGTT equaled 84 ± 2% (P = 0.003) of the response to the first OGTT. Absolute insulin secretion was lower (37.8 ± 4.3 vs. 42.8 ± 5.1 nmol/m², P = 0.02), but glucose potentiation (i.e., higher secretion at the same glycemia) was stronger (1.08 ± 0.02- vs. 0.92 ± 0.02-fold, P = 0.006), the increment being higher in Study II (+36 ± 5%) than Study I (+19 ± 6%, P < 0.05). In pooled data, a higher glucose area during the first OGTT was associated with a higher potentiation during the second OGTT (rho=0.60, P = 0.002). Neither insulin clearance nor glucose clearance differed between loads, and appearance of glucose over 3 h totalled 60 ± 6 g for the first load and 52 ± 5 g for the second load (P = not significant). Fasting endogenous glucose production [13.3 ± 0.6 µmol·min^–1·kg fat-free mass (FFM)^–1] averaged 6.0 ± 3.8 µmol·min^–1·kg FFM^–1 between 0 and 180 min and 1.7 ± 2.6 between 180 and 360 min (P < 0.03). Glucose potentiation and stronger suppression of endogenous glucose release are the main mechanisms underlying the Staub-Traugott effect.

glucose potentiation; glucose absorption; glucose tolerance