Gestational Glucose Tolerance Status May Affect Diabetes Risk
Early postpartum metabolic changes vary by gestational glucose tolerance status
THURSDAY, Aug. 12 (HealthDay News) -- β-cell dysfunction progresses in women with a history of gestational diabetes mellitus (GDM) and gestational impaired glucose tolerance (GIGT) in the first year after giving birth, and may contribute to subsequent development of type 2 diabetes, according to research published in the August issue of Diabetes Care.
Ravi Retnakaran, M.D., of Mount Sinai Hospital in Toronto, and colleagues gave a glucose challenge test (GCT) and an oral glucose tolerance test (OGTT) to 392 pregnant women, followed by an OGTT at three and 12 months' postpartum. Their objective was to determine whether the metabolic changes that happen in the first year after giving birth vary by gestational glucose tolerance status.
The researchers found that the prevalence of dysglycemia increased progressively from those with normal GCT with normal glucose tolerance (NGT) to abnormal GCT NGT to GIGT to GDM both three and 12 months' postpartum. The four groups varied markedly with regards to changes in β-cell function, with Insulin Secretion-Sensitivity Index-2 (ISSI-2) falling in the GDM and GIGT groups. Further analysis revealed GDM and GIGT status as independent negative predictors of ISSI-2 changes between three and 12 months' postpartum. The authors conclude that declining β-cell function in the first year after giving birth in women with GDM and GIGT likely contributes to a future risk of developing type 2 diabetes.
"In summary, the pattern of change in β-cell function in the first year postpartum varies in relation to glucose tolerance status in pregnancy unlike changes in waist circumference, weight, and insulin sensitivity. Indeed, both GDM and GIGT independently predict declining β-cell function between three and 12 months' postpartum. It thus emerges that β-cell dysfunction progresses in the early postpartum in women with a history of gestational dysglycemia and is likely a pathophysiologic factor contributing to the development of type 2 diabetes in this at-risk patient population," the authors write.