Effects of type 2 diabetes on Insulin Secretion, Insulin Action, Glucose Effectiveness and Postprandial Glucose Metabolism

  1. Ananda Basu, MD (basu.ananda{at}mayo.edu),
  2. Chiara Dalla Man, PhD*,
  3. Rita Basu, MD,
  4. Gianna Toffolo, PhD*,
  5. Claudio Cobelli, PhD* and
  6. Robert A. Rizza, MD
  1. Division of Endocrinology and Metabolism, Mayo Clinic College of Medicine, 200, First Street SW, Rochester, MN 55905
  2. *Department of Information Engineering, University of Padova, Padova, Italy

    Abstract

    Objective: This study sought to determine whether postprandial insulin secretion, insulin action, glucose effectiveness and glucose turnover were abnormal in type 2 diabetes.

    Research Design: 14 subjects with type 2 diabetes and 11 non-diabetic subjects matched for age, weight and body mass index underwent a mixed meal test using the triple tracer technique. Indices of insulin secretion, insulin action, and glucose effectiveness were assessed using the oral “minimal” and C-peptide models.

    Results: Fasting and postprandial glucose concentrations were higher in the diabetic than non-diabetic subjects. Although peak insulin secretion was delayed (p<0.001) and lower (p<0.05) in type 2 diabetes, integrated total postprandial insulin response did not differ between groups. Insulin action, insulin secretion, disposition indices and glucose effectiveness all were lower (p<0.05) in diabetic than non-diabetic subjects. Whereas the rate of meal glucose appearance did not differ between groups, the percent suppression of EGP was slightly delayed and increment in glucose disappearance was substantially lower (p<0.01) in diabetic subjects during the first three hours after meal ingestion. Together, these defects resulted in an excessive rise in postprandial glucose concentrations in the diabetic subjects.

    Conclusion: When measured using methods that avoid non-steady error, the rate of appearance of ingested glucose was normal and suppression of EGP only minimally impaired. However, when considered in light of prevailing glucose concentration, both were abnormal. In contrast, rates of postprandial glucose disappearance were substantially decreased due to defects in insulin secretion, insulin action, and glucose effectiveness.

    Footnotes

      • Received October 7, 2008.
      • Accepted January 20, 2009.