Abstract

resistance in mid pregnancy and neonatal birth weight in uncomplicated pregnancies Hiroshi Yamashita, Masashi Fukuda, Yukari Kugishima, Yuki Yamauchi, Akiko Kuzume, Takashi Hashimoto, So Sugimi, Naoko Yatsunami, Sachie Suga, Nobuko Kusuda, Ichiro Yasuhi Nagasaki Medical Center, Obstetrics and Gynecology, Omura-city, Japan OBJECTIVE: The purpose of this study was to determine whether maternal insulin resistance measured by homeostasis model assessmentinsulin resistance (HOMA-IR) in mid pregnancy is associated with neonatal birth weight in uncomplicated pregnancies. STUDY DESIGN: We included singleton pregnant women who had a 75g oral glucose tolerance test (OGTT) during mid pregnancy because of a positive gestational diabetes (GDM) screen. We measured HOMA-IR derived from fasting plasma glucose and immuno-reactive insulin concentration at OGTT. Women with GDM, hypertension, or fetal malformation were excluded. Using multiple and logistic regression analysis to adjust for confounding variables including maternal age, prepregnancy body mass index (BMI), plasma glucose levels at OGTT, and gestational age (GA) at delivery, we tested the relation of mid pregnancy maternal HOMA-IR to neonatal birth weight and large for GA (LGA) infants. RESULTS: We included 557 Japanese pregnant women. The mean maternal age, prepregnancy BMI, GA at OGTT, and HOMA-IR, GA at delivery, and birth weight were 31.8 / 5.0 years, 22.0 / 3.7 kg/ m2, 30.5 / 4.0 weeks, and 1.46 / 0.8, 39.0 / 1.7 weeks, and 3,030 / 470 g, respectively. HOMA-IR was positively associated with birth weight after controlling confounding variables (p .05). Higher HOMA-IR was significantly associated with an increased incidence of LGA infants (n 38) with the adjusted odds ratio of 1.71 per one unit of HOMA-IR (95% confidence interval, 1.11-2.66). CONCLUSION: Our findings suggest that the degree of maternal insulin resistance measured by HOMA-IR during mid pregnancy is associated with birth weight in uncomplicated pregnancies. Mid pregnancy HOMA-IR could be a predictor of fetal overgrowth, independent of maternal glucose levels and obesity.

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