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Do Early Elevations in Amniotic Fluid Glucose and Insulin Predict the Risk for Gestational Diabetes Mellitus (GDM)?
Author(s) -
Tisi Daniel Kevin,
Burns David H,
Koski Kristine G
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a184-c
Subject(s) - gestational diabetes , medicine , amniotic fluid , insulin , offspring , obstetrics , amniocentesis , diabetes mellitus , pregnancy , endocrinology , fetus , gestation , prenatal diagnosis , biology , genetics
Screening and diagnosis for Gestational Diabetes Mellitus (GDM) is based on a series of abnormal oral glucose tolerance tests between 24–28 weeks in pregnant mothers. However, literature suggests that fetal metabolism might be perturbed earlier. Measuring fetal metabolomics using amniotic fluid (AF) may provide a window into this early in‐utero environment. Our objectives were (1) to determine if women subsequently diagnosed with GDM had elevated amniotic fluid (AF) glucose, insulin or insulin‐like‐growth‐factor‐binding‐protein 1 (IGFBP1) at the time of routine amniocentesis (12–22 wks) and (2) to quantify those amniotic fluid concentrations associated with increased risk for GDM using probability mapping. No women with pre‐existing diabetes were included. AF glucose and insulin were higher and IGFBP1 lower in women later diagnosed with GDM (p<0.01). Multiple logistic regression showed that maternal BMI, AF glucose, insulin and IGFBP1 were associated with later GDM diagnosis (p<0.05). Probability maps demonstrated that if high AF glucose (>144mg/mL) accompanied low IGFBP1 (< 20 mg/mL), GDM risk approached 80%. Interestingly, a greater GDM risk existed if either insulin or glucose was low and the other concentration elevated. We conclude that AF environment is sensitive to early fetal metabolic perturbations associated with GDM. This exposure to early elevations in AF glucose may provide an explanation for the inability of current GDM interventions to decrease the higher prevalence of NIDDM and GDM in adult GDM offspring. (Supported by Canadian Institutes for Health Research ‐ CIHR)