Contributions of Fasting and Postprandial Plasma Glucose Increments to the Overall Diurnal Hyperglycemia of Type 2 Diabetic Patients

Variations with increasing levels of HbA1c

  1. Louis Monnier, MD1,
  2. Hélène Lapinski, MD1 and
  3. Claude Colette, PHD2
  1. 1Department of Metabolism, Lapeyronie Hospital, Montpellier, France
  2. 2University Institute of Clinical Research, Montpellier, France


    OBJECTIVE—The exact contributions of postprandial and fasting glucose increments to overall hyperglycemia remain controversial. The discrepancies between the data published previously might be caused by the interference of several factors. To test the effect of overall glycemic control itself, we analyzed the diurnal glycemic profiles of type 2 diabetic patients investigated at different levels of HbA1c.

    RESEARCH DESIGN AND METHODS—In 290 non–insulin- and non–acarbose-using patients with type 2 diabetes, plasma glucose (PG) concentrations were determined at fasting (8:00 a.m.) and during postprandial and postabsorptive periods (at 11:00 a.m., 2:00 p.m., and 5:00 p.m.). The areas under the curve above fasting PG concentrations (AUC1) and >6.1 mmol/l (AUC2) were calculated for further evaluation of the relative contributions of postprandial (AUC1/AUC2, %) and fasting [(AUC2 − AUC1)/AUC2, %] PG increments to the overall diurnal hyperglycemia. The data were compared over quintiles of HbA1c.

    RESULTS—The relative contribution of postprandial glucose decreased progressively from the lowest (69.7%) to the highest quintile of HbA1c (30.5%, P < 0.001), whereas the relative contribution of fasting glucose increased gradually with increasing levels of HbA1c: 30.3% in the lowest vs. 69.5% in the highest quintile (P < 0.001).

    CONCLUSIONS—The relative contribution of postprandial glucose excursions is predominant in fairly controlled patients, whereas the contribution of fasting hyperglycemia increases gradually with diabetes worsening. These results could therefore provide a unifying explanation for the discrepancies as observed in previous studies.


    • Address correspondence and reprint requests to Prof. L. Monnier, Department of Metabolism, Lapeyronie Hospital, 34295 Montpellier Cedex 5, France. E-mail: l-monnier{at}

      Received for publication 29 March 2002 and accepted in revised form 20 November 2002.

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