Abstract
Aims The objective of the present study was to explore the long-term postpartum glucose metabolism in women with previous GDM, and study the mechanism of hyperglycemia from gestation to postpartum by investigating the postpartum insulin resistance and insulin secretion. Methods A total of 321 females with previous GDM were followed up once during 1- to 6-years postpartum. Characteristics during pregnancy, perinatal period, and postpartum were compared between postpartum NGT and hyperglycemic women. HOMA-IR and HOMA-β were used to assess insulin resistance and insulin secretion levels with different glucose statuses. Results The prevalence of postpartum hyperglycemia had a fluctuant increase from 25.9% at 1 year, to 53.7% at 5 year. 75 g OGTT 2 hPG during pregnancy was an independent predictor of postpartum hyperglycemia with an OR of 2.15 (95% CI 1.245, 3.722) (P=0.006). After ROC analysis, the best equilibrium between sensitivity (70.3%) and specificity (60.4%) for 2 hPG was 9.03 mmol/L. HOMA-IR was increased in postpartum normal glucose tolerance (NGT), prediabetes, and T2DM (1.64 vs. 2.14 vs. 4.27, P=0.006). After ROC analysis, the best equilibrium between sensitivity (70.3%) and specificity (60.4%) for 2 hPG was 9.03 mmol/L. HOMA-IR was increased in postpartum normal glucose tolerance (NGT), prediabetes, and T2DM (1.64 vs. 2.14 vs. 4.27, β were used to assess insulin resistance and insulin secretion levels with different glucose statuses. P=0.006). After ROC analysis, the best equilibrium between sensitivity (70.3%) and specificity (60.4%) for 2 hPG was 9.03 mmol/L. HOMA-IR was increased in postpartum normal glucose tolerance (NGT), prediabetes, and T2DM (1.64 vs. 2.14 vs. 4.27, β were used to assess insulin resistance and insulin secretion levels with different glucose statuses. Conclusions 75 g OGTT 2h PG during pregnancy higher than 9.03 mmol/L is regarded as an independent risk factor of postpartum hyperglycemia. Insulin resistance with insufficient insulin secretion compensation is still common phenomenon during long-term postpartum. Women with heavier insulin resistance in the postpartum period are more likely develop prediabetes, while decreased β-cell function contributes more to T2DM development.β were used to assess insulin resistance and insulin secretion levels with different glucose statuses.
Highlights
Gestational diabetes mellitus (GDM) is a common metabolic disorder during pregnancy, which is usually diagnosed in the second and third trimesters of pregnancy and is not overt diabetes [1]
Compared to women with normoglycemia during pregnancy, women with previous GDM are more likely to have the risk of developing postpartum type 2 diabetes mellitus (T2DM) (RR 7.43, 95% CI 4.79–11.51) [4]. is indicated that GDM might share similar pathogenesis with T2DM, and both are related to insulin resistance and insufficient β-cell function [9]
Before April 2011, the criteria put forwarded by the National Diabetes Date Group (NDDG) were used for diagnosing GDM. is method consisted of two steps, a 50 g glucose challenge test (GCT) and a 75 g oral glucose tolerance test (OGTT) during 24–28 weeks of gestation
Summary
Gestational diabetes mellitus (GDM) is a common metabolic disorder during pregnancy, which is usually diagnosed in the second and third trimesters of pregnancy and is not overt diabetes [1]. E adverse effects of GDM in mothers as well as offspring do not end with pregnancy termination. Several studies [4,5,6,7,8] have proved that both mothers and offspring have increased risk of metabolic disorders in the long term. Compared to women with normoglycemia during pregnancy, women with previous GDM are more likely to have the risk of developing postpartum type 2 diabetes mellitus (T2DM) (RR 7.43, 95% CI 4.79–11.51) [4]. Is indicated that GDM might share similar pathogenesis with T2DM, and both are related to insulin resistance and insufficient β-cell function [9]. GDM develops in women when there is excessive insulin resistance, inadequate
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