The Impact of Family History of Diabetes on Risk Factors for Gestational Diabetes

Summary
Objective: Familial history of type 2 diabetes (FHD) represents a pathophysiologically unique risk factor for gestational diabetes (GDM), insofar as it encompasses both inherited and lifestyle elements. We thus hypothesized that the risk factors for gestational hyperglycaemia in women with FHD may differ from those in women without FHD.
Design/patients/measurements: GDM risk factors were evaluated in 90 women with FHD and in 83 women without FHD, at the time of oral glucose tolerance testing in late pregnancy.
Results: There were no significant differences between the two groups in ethnicity, prepregnancy BMI, the insulin-sensitizing protein adiponectin, glucose tolerance status and area-under-the-glucose-curve (AUCgluc). In women with FHD, a multiple linear regression model of established GDM risk factors reconciled 35% of the variance in AUCgluc, with (i) previous GDM (t = 3.74, P = 0.0003) identified as a positive independent determinant and (ii) log adiponectin (t = -3.48, P = 0.0008) and, unexpectedly, parity (t = -3.19, P = 0.0021) emerging as negative independent covariates of AUCgluc. In contrast, in women without FHD, the same multivariate model reconciled only 15% of the variance in AUCgluc, with no significant variables identified. Interestingly, in the entire population (n = 173), parity significantly modified the relationship between FHD and AUCgluc (FHD-parity interaction: t = -2.29, P = 0.0235). Indeed, FHD was an independent determinant of AUCgluc in nulliparous women (n = 91), but not in parous women (n = 82).
Conclusion: Established risk factors for GDM are relevant in women with FHD but may not be the principal determinants of gestational hyperglycaemia in women without FHD. Moreover, FHD may be more relevant to risk of GDM in nulliparous women than in parous subjects. These findings highlight the complex relationship between FHD and gestational hyperglycaemia, and may hold implications for selective screening for GDM.

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Clin Endocrinol. 2007;67(5):754-760. ©2007 Blackwell Publishing
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