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

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 (dAUCGL) and C-peptide (dAUCCP) evaluated BC during OGTT (BCOG) and IVGTT (BCIV). Incretin effect was computed in all fGDM and in fGDM with normal tolerance (fGDMNGT) and with impaired glucose regulation (fGDMIGR). Results. dAUCGL of fGDM was higher (P < 0.0001) than CNT for both tests; while dAUCCP were not different. BCOG and BCIV were lower in fGDM versus CNT (1.42 ± 0.17nmolCP/mmolGLUC 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 fGDMNGT (60 ± 3), but higher than that of fGDMIGR (52 ± 6; P = 0.03). IE normalized to BMI was 2.77 ± 0.19 % m2/kg in CNT, higher than that of fGDMIGR (1.75 ± 0.21; P = 0.02) and also of fGDMNGT  (2.33 ± 0.11; P = 0.038). Conclusion. Compromised IE characterizes fGDMIGR. 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

PRKAR1A mutation causing pituitary-dependent Cushing disease in a patient with Carney complex

“Disclaimer: this is not the definitive version of record of this article. This manuscript has been accepted for publication inEuropean Journal of Endocrinology, but the version presented here has not yet been copy-edited, formatted or proofed. Consequently, Bioscientifica accepts no responsibility for any errors or omissions it may contain. The definitive version is now freely available at https://doi.org/10.1530/EJE-17-0227 2017.

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

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 &lt; 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