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International Journal of Endocrinology
Volume 2012, Article ID 247392, 4 pages
Clinical Study

Incretin Effect in Women with Former Gestational Diabetes within a Short Period after Delivery

1Metabolic Unit, Institute of Biomedical Engineering, National Research Council, 35127 Padova, Italy
2Department of Internal Medicine III, Medical University of Vienna, 1090 Vienna, Austria

Received 31 December 2011; Accepted 28 February 2012

Academic Editor: Yariv Yogev

Copyright © 2012 G. Pacini et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background and Aims. Women with former gestational diabetes (fGDM) are characterized by impaired beta-cell function (BC). Incretin hormones contribute to insulin secretion after oral administration of glucose. We aimed to assess the possible role of incretins on altered insulin release in fGDM. Materials and Methods. We studied 104 fGDM women within 6 months after delivery and 35 healthy women after normal pregnancy (CNT) with a 75 g oral (OGTT) and a 0.33 g/kg intravenous (IVGTT) glucose test, both lasting 3 h. The ratio of suprabasal areas under the concentration curves for glucose ( ) and C-peptide ( ) evaluated BC during OGTT ( ) and IVGTT ( ). Incretin effect was computed in all fGDM and in fGDM with normal tolerance ( ) and with impaired glucose regulation ( ). Results. of fGDM was higher ( ) than CNT for both tests; while were not different. and were lower in fGDM versus CNT ( / versus , and versus , , respectively). IE in CNT (  %) was not different from that of all fGDM ( ) and ( ), but higher than that of ( ; ). IE normalized to BMI was  % m2/kg in CNT, higher than that of ( ; ) and also of ( ; ). Conclusion. Compromised IE characterizes . In both fGDM categories, regardless their glucose tolerance, IE normalized to BMI was reduced, signifying an intrinsic characteristic of fGDM. Therefore, the diminished IE of fGDM seems to reflect an early abnormality of the general beta-cell dysfunction in the progression toward type 2 diabetes.