ECE2016 Eposter Presentations Diabetes (to include epidemiology, pathophysiology) (83 abstracts)
Universitary Hospital Virgen de la Victoria, Málaga, Spain.
Introduction: There is a reduction of the incretin effect in patients with type 2 diabetes secondary to altered secretion of incretin hormones and/or failed of its action.
Objective: To study the GLP-1 secretion pattern after an oral glucose tolerance test (OGTT) in postpartum reassessment of women with previous GDM.
Materials and methods: Prospective epidemiological study of 48 women with a history of GDM. We evaluated age, history of GDM or macrosomia, family history of diabetes, insulin therapy use, birth weight and type of delivery; 13±1 months after childbirth, we reassessed clinical-analytical characteristics and performed a 75-g OGTT. We measured glucose, insulin and GLP-1 levels (basal-30-60-120′). Classification of patients was based on OGTT: normal vs prediabetic/diabetic and based on BMI: obese (IMC≥30 kg/m2) vs non-obese. Differences between groups were analyzed using MannWhitney and χ2 tests.
Results: Patients mean age 35±5 years, BMI 29±6 kg/m2, A1c 5.5±0.3%, HOMA-IR 2.2±1.4. Women with pathological OGTT needed insulin therapy more often during pregnancy and had higher levels of insulin resistance, but they did not differ significantly from those with non-pathological OGTT in metabolic syndrome characteristics although they had higher cholesterol and triglycerides levels. There were no significant differences in GLP-1 basal levels and after the OGTT between groups. Obese women had significantly higher basal and postprandial insulin, HOMA-IR and HOMA-β with no differences in glucose levels, and lower levels of basal and postprandial GLP-1 than non-obese.
Conclusions: Women with a history of GDM and prediabetes/diabetes in postpartum reassessment do not differ in GLP-1 secretion after OGTT of healthy patients. However, obese patients have lower incretinic response after OGTT compared with non-obese.
The defect in incretinic secretion does not help to explain the pathogenesis of diabetes that occurs after GDM.