Abstract
BackgroundInsulin resistance and beta cell dysfunction were reported to be responsible for gestational diabetes mellitus (GDM). However, little is known about the heterogeneity of these factors and its influences on perinatal outcomes. We investigated whether subtypes of insulin resistance and beta cell dysfunction in gestational diabetes mellitus have different impacts on perinatal outcomes.MethodsIn this prospective cohort study, we followed 554 pregnant women and glucose challenge test was performed at 24–28th weeks of their gestation. Women with plasma glucose ≥ 7.8 mmol/L would be included and advised to undergo the diagnostic 75-g, 3-h oral glucose tolerance test. According to indices of measuring insulin resistance or beta cell function were below the 25th percentile of women with normal glucose tolerance (NGT), women with GDM were defined as three subtypes: GDM with the beta cell dysfunction, GDM with the insulin resistance defect or GDM with both traits mentioned above (GDM-mixed). Perinatal outcomes were documented.ResultsThe levels of prepregnancy and maternal BMI in the GDM-mix group were higher compared to women in the NGT group (23.2 ± 4.0 vs 20.8 ± 3.7 kg/m2, P < 0.001; 24.5 ± 4.3 vs 21.8 ± 3.4 kg/m2, P < 0.001, respectively). Furthermore, women in GDM-mix group more likely to be subjected to LGA (P = 0.008) adverse perinatal outcomes (P = 0.005), although these differences were normalized after adjusting age, prepregnancy and maternal BMI (GDM-mix vs. NGT: P = 0.141 for LGA and P = 0.186 for adverse outcomes). On the other hand, all perinatal outcomes were similar between other two GDM subgroups and NGT group.ConclusionsWomen with GDM display respective characteristics on metabolism disorders and confer discriminating risks of adverse perinatal outcomes because of this heterogeneity.
Highlights
Insulin resistance and beta cell dysfunction were reported to be responsible for gestational diabetes mellitus (GDM)
35 women were classified into GDM-resistance group. 43 women were eligible for the GDM-dysfunction group and 79 women, commodity with insulin resistance and beta cell dysfunction, were in the GDM-mix group
Among different subtypes in GDM, women in the GDM-mix group were older than women with normal glucose tolerance (NGT) (32 ± 6.0 vs 29 ± 5.0 years, P < 0.001) and the levels of prepregnancy and maternal body mass index (BMI) were much higher compared to women in the NGT group (23.2 ± 4.0 vs 20.8 ± 3.7 kg/m2, P < 0.001; 24.5 ± 4.3 vs 21.8 ± 3.4 kg/m2, P < 0.001, respectively)
Summary
Insulin resistance and beta cell dysfunction were reported to be responsible for gestational diabetes mellitus (GDM). Exact mechanisms responsible for the development of hyperglycemia during pregnancy are not fully understood, insulin resistance has been identified as the catalyst of GDM with advancing gestation. Chronic inflammation factors, such as tumor necrosis factor α, and placental-derived hormones, such as placental lactogen and growth hormone, have been verified to be contributors to this increasing level of insulin resistance [6, 7] and when women fail to adapt to these physiological changes, they develop the glucose intolerance during pregnancy. We carried out a prospective cohort study to clarify the heterogeneous impact of insulin resistance and beta cell dysfunction in GDM on perinatal outcomes
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