Background: Maternal overweight is a risk factor for Gestational Diabetes Mellitus (GDM) . However, there is emerging evidence that increased maternal BMI has considerable impact on the development of large for gestational age (LGA) offspring even in women who do not develop GDM, possibly related to subtle impairments in glucose metabolism. This study aims to assess physiological changes associated with increased BMI.

Methods: 21 women with overweight and 21 normal weight controls were included in this explorative study and received a metabolic assessment at early pregnancy (13.3 weeks) (Visit 1) , including a 60 min frequently sampled intravenous glucose tolerance test (FSIGT) . An OGTT was performed between 24 and 28 weeks of gestation (Visit 2) in women who remained normal glucose tolerant.

Results: At V1 mothers with overweight showed significantly elevated fasting glucose and HbA1c values, a well as impaired insulin sensitivity at fasting condition and dynamically assessed during the FSIGT, whereby the Calculated Insulin Sensitivity index (CSI) was lower in the overweight group as compared to normal weight controls (3.5 vs. 6.7 10-4⋅[μU/mL]-1⋅min-1, p=0.025) . The Disposition Index (DI) as a parameter of β-cell function was significantly decreased in mothers with overweight. Likewise, maternal BMI was inversely related to fasting (rho=0.56, p=0.005) and dynamically assessed insulin sensitivity (rho=0.51, p=0.014) as well as the DI (rho=0.51, p=0.014) and the AUC of glucose (rho=0.66, p<0.001) and C-Peptide (rho=0.46, p=0.020) during the OGTT in mothers who remained normal glucose tolerant during pregnancy at V2.

Conclusions: Increased maternal BMI is associated to insulin resistance and impaired β-cell function already at early pregnancy. We also observed that maternal BMI was associated with impaired glucose metabolism and especially elevated glucose levels during the OGTT at mid gestation in women who did not develop GDM and remained normal glucose tolerant.


T.Linder: None. D.Eppel: None. C.Monod: None. G.Kotzaeridi: None. A.Tura: None. C.S.Göbl: Research Support; Dexcom, Inc., Sanofi.

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