Abstract

OBJECTIVE—To test the hypothesis that elevated midpregnancy serum insulin (IRI) and C-peptide (CP) concentrations are associated with later development of pregnancy-induced hypertension (PIH), independent of prepregnancy obesity and midpregnancy blood pressure.

RESEARCH DESIGN AND METHODS—In this prospective study, a cohort of normotensive women, ages ≥18 years, performed a 50-g glucose challenge test at 24–30 weeks’ gestational age. Blood samples were collected after an overnight fast and 1 h after glucose ingestion. Serum IRI and CP concentrations were measured in each sample. Maternal height, blood pressure, and proteinuria were measured at the time of glucose challenge testing and after 36 weeks’ gestational age.

RESULTS—Of 320 subjects enrolled, 44 women (13.8%) had subsequent PIH. Crude odds ratios (ORs) for development of PIH associated with each 1 U rise in log fasting IRI, log fasting CP, and glucose-induced increase in CP (expressed as log [postprandial CP/fasting CP]) were 2.0 (95% CI 1.3–3.3), 1.8 (CI 1.2–2.7), and 2.3 (CI 1.1–4.9), respectively. After controlling for prepregnancy BMI, gestational age, and midpregnancy mean arterial pressure, adjusted ORs corresponding to log fasting IRI and CP for the development of PIH were 1.3 (95% CI 0.7–2.3) and 1.7 (CI 1.1–2.7), respectively, and, after adjustment for fasting CP, the adjusted OR of the glucose-induced rise in log CP was 3.7 (CI 1.5–9.3).

CONCLUSIONS—Mid-pregnancy fasting and postoral glucose CP levels are associated with subsequent development of PIH, independent of maternal obesity and midpregnancy baseline blood pressure. These findings may reflect an amplified β-cell response to glycemic stimulus, similar to that found in states of insulin resistance, that appears to be independently associated with PIH.