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 (dAUC(GL)) and C-peptide (dAUC(CP)) evaluated BC during OGTT (BC(OG)) and IVGTT (BC(IV)). Incretin effect was computed in all fGDM and in fGDM with normal tolerance (fGDM(NGT)) and with impaired glucose regulation (fGDM(IGR)). Results. dAUC(GL) of fGDM was higher (P < 0.0001) than CNT for both tests; while dAUC(CP) were not different. BC(OG) and BC(IV) were lower in fGDM versus CNT (1.42 ± 0.17nmol(CP)/mmol(GLUC) versus 2.53 ± 0.61, P = 0.015 and 0.41 ± 0.03 versus 0.68 ± 0.10, P = 0.0006, respectively). IE in CNT (66 ± 4 %) was not different from that of all fGDM (59 ± 3) and fGDM(NGT) (60 ± 3), but higher than that of fGDM(IGR) (52 ± 6; P = 0.03). IE normalized to BMI was 2.77 ± 0.19 % m(2)/kg in CNT, higher than that of fGDM(IGR) (1.75 ± 0.21; P = 0.02) and also of fGDM(NGT )(2.33 ± 0.11; P = 0.038). Conclusion. Compromised IE characterizes fGDM(IGR). 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.